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Cancer prevention: 7 tips to reduce your risk

Concerned about cancer prevention? Take charge by making changes such as eating a healthy diet and getting regular screenings.

How do people lower the chances of getting cancer? There's plenty of advice. But at times, advice from one study goes against the advice from another.

Cancer prevention information continues to develop. However, it's well accepted that lifestyle choices affect the chances of getting cancer.

Consider these lifestyle tips to help prevent cancer.

1. Don't use tobacco

Smoking has been linked to many types of cancer, including cancer of the lung, mouth, throat, voice box, pancreas, bladder, cervix and kidney. Even being around secondhand smoke might increase the risk of lung cancer.

But it's not only smoking that's harmful. Chewing tobacco has been linked to cancer of the mouth, throat and pancreas.

Staying away from tobacco — or deciding to stop using it — is an important way to help prevent cancer. For help quitting tobacco, ask a health care provider about stop-smoking products and other ways of quitting.

2. Eat a healthy diet

Although eating healthy foods can't ensure cancer prevention, it might reduce the risk. Consider the following:

• Eat plenty of fruits and vegetables. Base your diet on fruits, vegetables and other foods from plant sources — such as whole grains and beans. Eat lighter and leaner by choosing fewer high-calorie foods. Limit refined sugars and fat from animal sources.
• Drink alcohol only in moderation, if at all. Alcohol increases the risk of various types of cancer, including cancer of the breast, colon, lung, kidney and liver. Drinking more increases the risk.
• Limit processed meats. Eating processed meat often can slightly increase the risk of certain types of cancer. This news comes from a report from the International Agency for Research on Cancer, the cancer agency of the World Health Organization.

People who eat a Mediterranean diet that includes extra-virgin olive oil and mixed nuts might have a reduced risk of breast cancer. The Mediterranean diet focuses mostly on plant-based foods, such as fruits and vegetables, whole grains, legumes and nuts. People who follow the Mediterranean diet choose healthy fats, such as olive oil, over butter. They eat fish instead of red meat.

3. Maintain a healthy weight and be physically active

Being at a healthy weight might lower the risk of some types of cancer. These include cancer of the breast, prostate, lung, colon and kidney.

Physical activity counts too. Besides helping control weight, physical activity on its own might lower the risk of breast cancer and colon cancer.

Doing any amount of physical activity benefits health. But for the most benefit, strive for at least 150 minutes a week of moderate aerobic activity or 75 minutes a week of hard aerobic activity.

You can combine moderate and hard activity. As a general goal, include at least 30 minutes of physical activity in your daily routine. More is better.

4. Protect yourself from the sun

Skin cancer is one of the most common kinds of cancer and one of the most preventable. Try these tips:

• Avoid midday sun. Stay out of the sun between 10 a.m. and 4 p.m. when the sun's rays are strongest.
• Stay in the shade. When outdoors, stay in the shade as much as possible. Sunglasses and a broad-brimmed hat help too.
• Cover your skin. Wear clothing that covers as much skin as possible. Wear a head cover and sunglasses. Wear bright or dark colors. They reflect more of the sun's harmful rays than do pastels or bleached cotton.
• Don't skimp on sunscreen. Use a broad-spectrum sunscreen with an SPF of at least 30, even on cloudy days. Apply a lot of sunscreen. Apply again every two hours, or more often after swimming or sweating.
• Don't use tanning beds or sunlamps. These can do as much harm as sunlight.

5. Get vaccinated

Protecting against certain viral infections can help protect against cancer. Talk to a health care provider about getting vaccinated against:

Hepatitis B. Hepatitis B can increase the risk of developing liver cancer. Adults at high risk of getting hepatitis B are people who have sex with more than one partner, people who have one sexual partner who has sex with others, and people with sexually transmitted infections.

Others at high risk are people who inject illegal drugs, men who have sex with men, and health care or public safety workers who might have contact with infected blood or body fluids.

• Human papillomavirus (HPV). HPV is a sexually transmitted virus that can lead to cervical cancer and other genital cancers as well as squamous cell cancers of the head and neck. The HPV vaccine is recommended for girls and boys ages 11 and 12. The U.S. Food and Drug Administration recently approved the use of the vaccine Gardasil 9 for males and females ages 9 to 45.

6. Avoid risky behaviors

Another effective cancer prevention tactic is to avoid risky behaviors that can lead to infections that, in turn, might increase the risk of cancer. For example:

Practice safe sex. Limit the number of sexual partners and use a condom. The greater the number of sexual partners in a lifetime, the greater the chances of getting a sexually transmitted infection, such as HIV or HPV .

People who have HIV or AIDS have a higher risk of cancer of the anus, liver and lung. HPV is most often associated with cervical cancer, but it might also increase the risk of cancer of the anus, penis, throat, vulva and vagina.

• Don't share needles. Injecting drugs with shared needles can lead to HIV, as well as hepatitis B and hepatitis C — which can increase the risk of liver cancer. If you're concerned about drug misuse or addiction, seek professional help.

7. Get regular medical care

Doing regular self-exams and having screenings for cancers — such as cancer of the skin, colon, cervix and breast — can raise the chances of finding cancer early. That's when treatment is most likely to succeed. Ask a health care provider about the best cancer screening schedule for you.

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• Cancer prevention overview (PDQ) — Patient version. National Cancer Institute. https://www.cancer.gov/about-cancer/causes-prevention/patient-prevention-overview-pdq. Accessed Oct. 24, 2022.
• Lewandowska AM, et al. Cancer prevention — Review paper. Annals of Agriculture and Environmental Medicine. 2021; doi:10.26444/aaem/116906.
• Colditz GA. Overview of cancer prevention. https://www.uptodate.com/contents/search. Accessed Oct. 24, 2022.
• Fletcher GS. Evidence-based approach to prevention. https://www.uptodate.com/contents/search. Accessed Oct. 24, 2022.
• Patel AV, et al. American College of Sports Medicine roundtable report on physical activity, sedentary behavior and cancer prevention and control. Medicine & Science in Sports & Exercise. 2019; doi:10.1249/MSS.0000000000002117.
• Health risks of smokeless tobacco. American Cancer Society. https://www.cancer.org/cancer/cancer-causes/tobacco-and-cancer/smokeless-tobacco.html. Accessed Oct. 24, 2022.
• Diet and physical activity: What's the cancer connection? American Cancer Society. https://www.cancer.org/cancer/cancer-causes/diet-physical-activity/diet-and-physical-activity.html. Accessed Oct. 24, 2022.
• Physical activity and cancer. National Cancer Institute. https://www.cancer.gov/about-cancer/causes-prevention/risk/obesity/physical-activity-fact-sheet. Accessed Oct. 24, 2022.
• HPV vaccines. American Cancer Society. https://www.cancer.org/cancer/cancer-causes/infectious-agents/hpv/hpv-vaccines.html. Accessed Oct. 24, 2022.
• How do I protect myself from ultraviolet (UV) rays? American Cancer Society. https://www.cancer.org/healthy/be-safe-in-sun/uv-protection.html. Accessed Oct. 24, 2022.
• Recommended vaccines for healthcare workers. Centers for Disease Control and Prevention. https://www.cdc.gov/vaccines/adults/rec-vac/hcw.html. Accessed Oct. 24, 2022.
• Cancers caused by HPV. Centers for Disease Control and Prevention. https://www.cdc.gov/hpv/parents/cancer.html?CDC_AA_refVal=https%3A%2F%2Fwww.cdc.gov%2Fhpv%2Fcancer.html. Accessed Oct. 24, 2022.
• HIV infection and cancer risk. American Cancer Society. https://www.cancer.gov/about-cancer/causes-prevention/risk/infectious-agents/hiv-fact-sheet. Accessed Oct. 24, 2022.
• IARC Working Group on the Evaluation of Carcinogenic Risk to Humans. Vol. 114: Red meat and processed meat. In: IARC Monographs on the Evaluation of Carcinogenic Risk to Humans. Lyon, France: International Agency for Research on Cancer; 2018. https://monographs.iarc.fr/monographs-and-supplements-available-online/. Accessed Nov. 4, 2018.
• FDA approves expanded use of Gardasil 9 to include individuals 27 through 45 years old. U.S. Food and Drug Administration. https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm622715.htm. Accessed Oct. 24, 2022.

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Can cancer be prevented?

Not all cancers can be prevented but there are things you can do to reduce your risk.

These include not smoking and keeping a healthy weight.

The world around us can make being healthy hard, and this can affect some people more than others. We need the government to help make it easier for us all. 

How can making healthy changes reduce my cancer risk?

A person’s risk of cancer depends on many different things. Research shows that things like stopping smoking and keeping a healthy weight can reduce the risk of cancer. By making healthy changes now, you can make a difference to your health in the future.

Use this page to explore six things that can reduce cancer risk.

And remember, you can also talk to your doctor if you’re worried about your cancer risk.

Can I make sure I don’t get cancer?

No, but making healthy changes does help reduce the risk.  There are some things we can’t change that increase the risk of cancer. These include things like getting older and a family history of cancer. 

The world around us also affects how healthy we are. There are some things we can do to help us form healthy habits. But we also need the government to help make it easier for everyone to be healthy.

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Not smoking

Not smoking is the best thing you can do to reduce your risk of cancer.  Harmful chemicals in cigarette smoke affect the entire body, not just our lungs. If you smoke, the best thing you can do for your health is quit.

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Keep a healthy weight

Being a healthy weight has lots of health benefits, including reducing the risk of cancer. But the world around us can make this difficult, which is why the government needs to help too.

Have a healthy balanced diet

Having healthy food and drink can reduce your risk of cancer. Aim to have plenty of fruit and vegetables, wholegrain foods high in fibre and healthy proteins. Cut down on processed and red meat, alcohol and high calorie foods and drinks.

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Enjoy the sun safely

Being safe in the sun reduces the risk of skin cancer. Too much UV radiation from the sun or sunbeds damages our skin cells. When the sun is strong, take extra care to protect your skin- spend time in the shade, cover up with clothing, and use sunscreen.

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Cut back on alcohol

The HPV Vaccine

The HPV vaccine is offered for free to children aged 11-13, and some other groups. It helps protect against HPV infection, reducing the risk of some types of cancer. The vaccine has been proven to be safe and effective.  

How does cancer start?

DNA is a set of instructions inside our cells that tells them how to behave. Cancer is caused by damage to our DNA that has built up over time.

Some things can increase the chances of this, such as UV rays from the sun and drinking alcohol.

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Improved Strategies for Cancer Prevention and Early Detection

The prevention of cancer and the development of more effective strategies to detect cancer precursors and early-stage cancers, when treatment may be most effective, remain critical goals.

The time from initial exposure to a cancer-causing agent—for example, a carcinogen such as ultraviolet light or tobacco smoke, or an infectious agent such as human papillomavirus (HPV)—to the development of cancer typically takes decades. Consequently, it often takes many years before a decrease in exposure results in a reduction in cancer incidence and mortality. However, a decrease in exposure during this long interval can eventually result in substantial long-term dividends, as seen with the reduction in smoking rates that have contributed to the reduction in lung cancer incidence and mortality over the past 10 years.

Many preventive efforts are directed at reducing or eliminating exposures to carcinogens or protecting the body from exposures. Other efforts may involve screening procedures, such as those for cervical and colorectal cancers, which can detect premalignant lesions in individuals without symptoms who can be treated before cancer develops.

Although the pharmaceutical industry regularly funds diagnostic and therapeutically oriented research, the majority of prevention-oriented research is funded by the public sector because many preventive agents and interventions provide minimal or no potential for commercial profit. Nevertheless, prevention has the potential, in the long run, to save more lives from cancer than treatment—as is already true for tobacco use and lung cancer—which underlines the importance of strong support for this research area. Prevention can also preclude the potential physical and psychological morbidity of diagnosis and treatment.

Preventing Cancers Caused by Viral Infections

Identifying an infectious agent as a cause of cancer provides several paths to the possibility of prevention, including reducing or eliminating exposure to the agent, developing a vaccine that prevents infection, or treating the infection before cancer develops. The identification of hepatitis B virus (HBV) in the 1960s, and the recognition that chronic HBV infection is an important cause of serious liver disease, including liver cancer, led to development in the 1980s of the first vaccine that can prevent cancer. Recent developments with three oncogenic viruses— human papillomavirus (HPV), Epstein-Barr virus (EBV), and hepatitis C virus (HCV)—illustrate how research advances have the potential to substantially reduce cancers attributable to these respective agents.

Human Papillomavirus

HPV infection causes virtually all cases of cervical cancer and a substantial proportion of several other cancers. In the United States, the number of noncervical cancers attributable to HPV infection is similar to that of cervical cancers. Pap smear-based cervical cancer screening and treatment of identified premalignant lesions has contributed to an approximately 75 percent reduction in the incidence of and mortality from this cancer since the early 1950s.

On the other hand, there have been substantial increases in HPV-associated anal and oropharyngeal cancers, two diseases for which validated population-based screening has not been developed. The vast majority of anal cancers are caused by HPV infection, and anal cancer incidence and mortality increased by 26 percent and 33 percent, respectively, from 2003 through 2012. The incidence of HPV-positive oropharyngeal cancer increased more than threefold during a recent 25-year period, and it is estimated that by 2020, the number of HPV-positive oropharyngeal cancers in the United States will be greater than the number of cases of cervical cancer.

A safe and effective vaccine against HPV types 16 and 18, two oncogenic types of HPV that cause approximately 70 percent of cervical cancers, was approved by the FDA in 2006, followed in 2009 by the approval of a second vaccine that targets the same oncogenic HPV types. In 2014, a third vaccine that targets HPV types 16, 18, 31, 33, 45, 52, and 58 was approved by the FDA. If administered prior to HPV exposure, this third vaccine should, in principle, prevent up to 90 percent of cases of cervical cancer. Theoretically, all three vaccines should also help reduce the incidence of noncervical cancers attributable to HPV infection.

Research is already having a major impact on reducing the incidence of high-grade cervical dysplasia in young women in Australia, where there has been high vaccine uptake. However, these vaccines are underused in the United States, where only about 60 percent of teens have been vaccinated and a much smaller percentage have received the recommended three doses.

In most low- and middle-income countries, where cervical cancer is frequently the most common cancer among women, HPV vaccine program implementation has thus far been limited. As the President’s Cancer Panel noted in a recent report , the underuse of HPV vaccines is a serious threat to progress against cancer but one that can be addressed.

Recent research strongly suggests that two doses, and perhaps even a single dose, of the current vaccines may be sufficient to induce long-term protection in young adolescents. A randomized trial of two versus three doses of one of the FDA-approved vaccines is now underway, and the feasibility of a trial of one versus two doses is being explored. If confirmed to provide long-term protection, reducing the number of doses could make vaccination logistically easier and less expensive.

The recognition of HPV as a cause of several cancers is having an impact on research and clinical practice beyond vaccines, including the prevention of cancer after persistent HPV infection has occurred. HPV-based testing, which is more sensitive than traditional Pap testing for both forms of cervical cancer (squamous cell carcinomas and adenocarcinomas), has been approved by the FDA for use in cervical cancer screening, initially only in conjunction with the Pap test, and, in 2014, as a primary screening method. This screening approach has the potential to further reduce the incidence of and mortality from this cancer.

To reduce the incidence of anal cancer, NCI has initiated a large screening trial to determine whether the treatment of high-grade anal dysplasia identified by screening high-risk patients can reduce their likelihood of developing invasive anal cancer.

Epstein-Barr Virus

EBV is an oncogenic herpesvirus that infects more than 90 percent of the world’s population before they reach adulthood. Infection with EBV has been associated with several types of cancer, including Burkitt lymphoma (82 percent of cases), gastric carcinoma (9 percent of cases), Hodgkin lymphoma (46 percent of cases), and nasopharyngeal carcinoma (98 percent of cases), as well as with infectious mononucleosis and other serious medical conditions. EBV infection is thought to account for more than 200,000 new cases of cancer each year worldwide. Therefore, developing a prophylactic vaccine against EBV infection is a public health priority.

Several different approaches are being explored in developing an EBV vaccine. In one approach, NCI-supported researchers have prepared virus-like particles that contain a glycoprotein called gp350/220, which is found on the surface of infectious EBV particles and the surface of EBV- infected cells. EBV uses gp350/220 to bind to cells and infect them.

The virus-like particles are similar to EBV in shape and size, and they contain dense arrays of gp350/220 on their surface. When tested in mice, they induced strong, long-lasting antibody responses, marked by the production of antibodies that are able to block EBV infection in vitro . Currently, these virus-like particles are being optimized and tested in additional animal models.

Hepatitis C Virus

HCV infection is a major cause of liver cancer in the United States and throughout the world. Much of the 26-percent increase in liver cancer mortality in the United States from 2003 through 2012 is believed to be attributable to infection with this virus. The recognition that HCV is frequently transmitted by blood products led to effective screening methods that have dramatically reduced the incidence of transfusion-related HCV infection.

Although efforts to develop a preventive HCV vaccine have thus far been unsuccessful, there has been enormous progress in developing effective antiviral drugs for the treatment of chronic HCV infection. Several of these drugs, which induce sustained virologic responses (i.e., elininate detectable HCV in the blood), have been licensed by the FDA since 2011. Long-term follow-up of treated patients will be needed to verify that treatment with these drugs has reduced their risk of liver cancer and other serious liver disease.

These advances in treatment contributed to the 2013 United States Preventive Services Task Force recommendation that all individuals born between 1945 and 1965, a group at high risk of acquiring HCV from contaminated blood products, be screened once for HCV infection. Further research is needed to determine whether additional age groups would benefit from screening for HCV infection.

Preventing Cancers with Drugs

NCI has investigated many natural and synthetic compounds to see if they have chemopreventive properties—properties that help reduce the risk of various types of cancer. The two most notable successes arising from this research are the approvals by the FDA of the drugs tamoxifen (Nolvadex®) and raloxifene (Evista®) to reduce the risk of breast cancer in women at increased risk of the disease.

Evidence from several studies of people who have taken low-dose aspirin for many years shows a substantial reduction in the incidence of and mortality from several types of cancer, including colorectal and lung cancers. However, the adoption of long-term chemoprevention of cancer with aspirin has been limited by concerns about side effects, such as gastrointestinal bleeding and certain forms of stroke, especially in older individuals. NCI is collaborating with the National Institute on Aging on a 5-year study of aspirin’s preventive attributes and side effects in 19,000 people over the age of 70 in the United States and Australia (age 65 or older in U.S. African Americans and Hispanics), in hopes of providing information that will better guide the use of aspirin for chemoprevention.

As in cancer treatment, the genomic methods of precision medicine may help identify patients who are more or less likely to reduce their cancer risk by taking aspirin. For example, a recent international retrospective study of regular aspirin and/or nonsteroidal anti-inflammatory drug (NSAID) use, funded largely by NCI, suggested that the risk of colorectal cancer differed among study participants based on genetic variation at two chromosomal locations, one on chromosome 12 and the other on chromosome 15. Participants who had specific genetic variants at the chromosome 12 location had decreased risks of colorectal cancer with regular aspirin and/or NSAID use, whereas participants with the other possible variants at this location had increased risks of the disease. Similarly, participants who had a specific genetic variant at the chromosome 15 location had decreased risks of colorectal cancer; however, the other possible genetic variants at this location were not associated with risk of the disease.

Identifying New Biomarkers for Risk and Early Detection of Cancer

For many years, scientists have been seeking to identify biological markers, or biomarkers, that accurately indicate increased risk of cancer or the presence of early-stage disease. The identification of increased risk may provide an opportunity for medical intervention to reduce risk, or heightened surveillance and early intervention as needed. Earlier cancer detection may permit earlier, more effective treatment and increase the chances of long-term survival. Biomarkers may also allow differentiation between cancers, precursor lesions that need to be treated, and precursor lesions that would never cause symptoms or threaten life and, therefore, do not need to be treated.

Biomarkers include genetic mutations, other changes in DNA, and abnormalities in proteins or other biological molecules that indicate the presence of an anomaly. They may be detected in blood, stool, other body fluids, or tissue. We know that inherited mutations in certain genes, such as BRCA1 and BRCA2 , which can be detected in blood samples, confer high risks of breast and ovarian cancers, but inherited mutations account for only a small percentage of all cancers that occur.

Although numerous biomarkers of cancer risk or malignant disease have been reported in the scientific literature in recent decades, very few have been validated or shown to be clinically useful. This fact led the Institute of Medicine and other organizations to develop recommendations and frameworks for cancer biomarker development.

These recommendations are crucial and timely because our ever-increasing understanding of the mechanisms of cancer, greatly facilitated by advanced genomic, proteomic, and other molecular technologies, is amplifying opportunities for cancer biomarker discovery and development. Moreover, biomarkers that reflect mechanisms related to cancer development or growth may suggest targeted chemoprevention to inhibit these mechanisms, which could form the basis of precision prevention and treatment.

New Candidate Biomarkers

Many malignant tumors shed entire cells, fragments of cells, and intracellular molecules into their immediate environment early in the disease process. Often these substances are detectable in the blood, other body fluids, or feces, providing the potential for easier, less-invasive screening methods for early cancer detection.

One type of biomarker that has been the focus of much interest lately is tumor cell DNA circulating in the blood, also known as circulating tumor DNA, or ctDNA. This DNA is marked by key mutations or other abnormalities found in the DNA of intact tumor cells.

In an international study involving 640 participants that was reported in 2014, researchers, including members of NCI’s Early Detection Research Network , used state-of-the-art molecular techniques to detect ctDNA in patients with various types of early-stage or late-stage cancer. Among patients with early-stage cancer, detectable ctDNA was found in 47 percent of those with stage I disease and 55 percent of those with stage II disease. Among patients with late-stage cancer, ctDNA was detected in 69 percent of the individuals with stage III disease and 82 percent of the individuals with stage IV disease.

Although these findings are promising, a number of technical challenges, including increasing the sensitivity of ctDNA detection, must be overcome before ctDNA assays can be applied clinically. Another challenge is that, theoretically, ctDNA may be released by a tumor before the tumor can be detected definitively with current imaging technologies, raising questions about how patients with detectable ctDNA but no tumor detectable by imaging would be managed medically.

Exosomes are another type of biomarker currently under investigation. They are extracellular, nano-sized vesicles (tiny membrane-enclosed cell fragments) that contain proteins, DNA, and RNA. All cells, including cancer cells, release exosomes. These tiny vesicles can enter the bloodstream and travel throughout body. Over the past decade, researchers have been exploring the use of exosomes as potential biomarkers for various diseases, including cancer.

In 2015, NCI-supported researchers reported that a protein called glypican 1 (GPC1), which is abundantly expressed on the surface of breast and pancreatic cancer cells, is also found on the surface of most exosomes derived from these cells. The presence of GPC1 on exosomes derived from normal breast and pancreatic cells is rare. The researchers then developed a method for detecting exosomes in blood and examined the blood of 190 patients with pancreatic cancer, 32 patients with breast cancer, and 100 healthy donors. In comparison with the healthy donors, all patients with pancreatic cancer and 75 percent of patients with breast cancer had higher levels of GPC1-containing exosomes in their blood.

Additional preliminary experiments suggest that GPC1 might be a marker for early pancreatic disease. Blood levels of GPC1-containing exosomes were consistently higher among five patients with pancreatic cancer precursor lesions than among healthy donors or 26 patients with benign pancreatic disease, such as chronic pancreatitis. The researchers validated their findings in an independent group of patients that included six with chronic pancreatitis, 56 with pancreatic cancer, and 20 healthy donors.

If these preliminary findings are confirmed, the results raise the possibility that a noninvasive screening test to detect pancreatic cancer early may be possible, opening the door to potentially curative surgery or the development of other new therapeutic interventions for more patients diagnosed with this frequently fatal disease.

The above-described research and applications, both realized and potential, represent only a small fraction of NCI’s efforts to advance cancer prevention and early detection. This work and these intriguing possibilities have been bolstered by our increasing knowledge and understanding of cancer and the advanced technologies that are ushering in the new era of precision medicine.

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Cancer Biology, Epidemiology, and Treatment in the 21st Century: Current Status and Future Challenges From a Biomedical Perspective

Patricia piña-sánchez.

1 Oncology Research Unit, Oncology Hospital, Mexican Institute of Social Security, Mexico

Antonieta Chávez-González

Martha ruiz-tachiquín, eduardo vadillo, alberto monroy-garcía, juan josé montesinos, rocío grajales.

2 Department of Medical Oncology, Oncology Hospital, Mexican Institute of Social Security, Mexico

Marcos Gutiérrez de la Barrera

3 Clinical Research Division, Oncology Hospital, Mexican Institute of Social Security, Mexico

Hector Mayani

Since the second half of the 20th century, our knowledge about the biology of cancer has made extraordinary progress. Today, we understand cancer at the genomic and epigenomic levels, and we have identified the cell that starts neoplastic transformation and characterized the mechanisms for the invasion of other tissues. This knowledge has allowed novel drugs to be designed that act on specific molecular targets, the immune system to be trained and manipulated to increase its efficiency, and ever more effective therapeutic strategies to be developed. Nevertheless, we are still far from winning the war against cancer, and thus biomedical research in oncology must continue to be a global priority. Likewise, there is a need to reduce unequal access to medical services and improve prevention programs, especially in countries with a low human development index.

Introduction

During the last one hundred years, our understanding of the biology of cancer increased in an extraordinary way. 1 - 4 Such a progress has been particularly prompted during the last few decades because of technological and conceptual progress in a variety of fields, including massive next-generation sequencing, inclusion of “omic” sciences, high-resolution microscopy, molecular immunology, flow cytometry, analysis and sequencing of individual cells, new cell culture techniques, and the development of animal models, among others. Nevertheless, there are many questions yet to be answered and many problems to be solved regarding this disease. As a consequence, oncological research must be considered imperative.

Currently, cancer is one of the illnesses that causes more deaths worldwide. 5 According to data reported in 2020 by the World Health Organization (WHO), cancer is the second cause of death throughout the world, with 10 million deaths. 6 Clearly, cancer is still a leading problem worldwide. With this in mind, the objective of this article is to present a multidisciplinary and comprehensive overview of the disease. We will begin by analyzing cancer as a process, focusing on the current state of our knowledge on 4 specific aspects of its biology. Then, we will look at cancer as a global health problem, considering some epidemiological aspects, and discussing treatment, with a special focus on novel therapies. Finally, we present our vision on some of the challenges and perspectives of cancer in the 21 st century.

The Biology of Cancer

Cancer is a disease that begins with genetic and epigenetic alterations occurring in specific cells, some of which can spread and migrate to other tissues. 4 Although the biological processes affected in carcinogenesis and the evolution of neoplasms are many and widely different, we will focus on 4 aspects that are particularly relevant in tumor biology: genomic and epigenomic alterations that lead to cell transformation, the cells where these changes occur, and the processes of invasion and metastasis that, to an important degree, determine tumor aggressiveness.

Cancer Genomics

The genomics of cancer can be defined as the study of the complete sequence of DNA and its expression in tumor cells. Evidently, this study only becomes meaningful when compared to normal cells. The sequencing of the human genome, completed in 2003, was not only groundbreaking with respect to the knowledge of our gene pool, but also changed the way we study cancer. In the post-genomic era, various worldwide endeavors, such as the Human Cancer Genome Project , the Cancer Genome ATLAS (TCGA), the International Cancer Genome Consortium, and the Pan-Cancer Analysis Working Group (PCAWG), have contributed to the characterization of thousands of primary tumors from different neoplasias, generating more than 2.5 petabytes (10 15 ) of genomic, epigenomic, and proteomic information. This has led to the building of databases and analytical tools that are available for the study of cancer from an “omic” perspective, 7 , 8 and it has helped to modify classification and treatment of various neoplasms.

Studies in the past decade, including the work by the PCAWG, have shown that cancer generally begins with a small number of driving mutations (4 or 5 mutations) in particular genes, including oncogenes and tumor-suppressor genes. Mutations in TP53, a tumor-suppressor gene, for example, are found in more than half of all cancer types as an early event, and they are a hallmark of precancerous lesions. 9 - 12 From that point on, the evolution of tumors may take decades, throughout which the mutational spectrum of tumor cells changes significantly. Mutational analysis of more than 19 000 exomes revealed a collection of genomic signatures, some associated with defects in the mechanism of DNA repair. These studies also revealed the importance of alterations in non-coding regions of DNA. Thus, for example, it has been observed that various pathways of cell proliferation and chromatin remodeling are altered by mutations in coding regions, while pathways, such as WNT and NOTCH, can be disrupted by coding and non-coding mutations. To the present date, 19 955 genes that codify for proteins and 25 511 genes for non-coding RNAs have been identified ( https://www.gencodegenes.org/human/stats.html ). Based on this genomic catalogue, the COSMIC (Catalogue Of Somatic Mutations In Cancer) repository, the most robust database to date, has registered 37 288 077 coding mutations, 19 396 fusions, 1 207 190 copy number variants, and 15 642 672 non-coding variants reported up to August 2020 (v92) ( https://cosmic-blog.sanger.ac.uk/cosmic-release-v92/ ).

The genomic approach has accelerated the development of new cancer drugs. Indeed, two of the most relevant initiatives in recent years are ATOM (Accelerating Therapeutics for Opportunities in Medicine), which groups industry, government and academia, with the objective of accelerating the identification of drugs, 13 and the Connectivity Map (CMAP), a collection of transcriptional data obtained from cell lines treated with drugs for the discovery of functional connections between genes, diseases, and drugs. The CMAP 1.0 covered 1300 small molecules and more than 6000 signatures; meanwhile, the CMAP 2.0 with L1000 assay profiled more than 1.3 million samples and approximately 400 000 signatures. 14

The genomic study of tumors has had 2 fundamental contributions. On the one hand, it has allowed the confirmation and expansion of the concept of intratumor heterogeneity 15 , 16 ; and on the other, it has given rise to new classification systems for cancer. Based on the molecular classification developed by expression profiles, together with mutational and epigenomic profiles, a variety of molecular signatures have been identified, leading to the production of various commercial multigene panels. In breast cancer, for example, different panels have been developed, such as Pam50/Prosigna , Blue Print , OncotypeDX , MammaPrint , Prosigna , Endopredict , Breast Cancer Index , Mammostrat, and IHC4 . 17

Currently, the genomic/molecular study of cancer is more closely integrated with clinical practice, from the classification of neoplasms, as in tumors of the nervous system, 18 to its use in prediction, as in breast cancer. 17 Improvement in molecular methods and techniques has allowed the use of smaller amounts of biological material, as well as paraffin-embedded samples for genomic studies, both of which provide a wealth of information. 19 In addition, non-invasive methods, such as liquid biopsies, represent a great opportunity not only for the diagnosis of cancer, but also for follow-up, especially for unresectable tumors. 20

Research for the production of genomic information on cancer is presently dominated by several consortia, which has allowed the generation of a great quantity of data. However, most of these consortia and studies are performed in countries with a high human development index (HDI), and countries with a low HDI are not well represented in these large genomic studies. This is why initiatives such as Human Heredity and Health in Africa (H3Africa) for genomic research in Africa are essential. 21 Generation of new information and technological developments, such as third-generation sequencing, will undoubtedly continue to move forward in a multidisciplinary and complex systems context. However, the existing disparities in access to genomic tools for diagnosis, prognosis, and treatment of cancer will continue to be a pressing challenge at regional and social levels.

Cancer Epigenetics

Epigenetics studies the molecular mechanisms that produce hereditable changes in gene expression, without causing alterations in the DNA sequence. Epigenetic events are of 3 types: methylation of DNA and RNA, histone modification (acetylation, methylation, and phosphorylation), and the expression of non-coding RNA. Epigenetic aberrations can drive carcinogenesis when they alter chromosome conformation and the access to transcriptional machinery and to various regulatory elements (promoters, enhancers, and anchors for interaction with chromatin, for example). These changes may activate oncogenesis and silence tumor-suppressor mechanisms when they modulate coding and non-coding sequences (such as micro-RNAs and long-RNAs). This can then lead to uncontrolled growth, as well as the invasion and metastasis of cancer cells.

While genetic mutations are stable and irreversible, epigenetic alterations are dynamic and reversible; that is, there are several epigenomes, determined by space and time, which cause heterogeneity of the “epigenetic status” of tumors during their development and make them susceptible to environmental stimuli or chemotherapeutic treatment. 22 Epigenomic variability creates differences between cells, and this creates the need to analyze cells at the individual level. In the past, epigenetic analyses measured “average states” of cell populations. These studies revealed general mechanisms, such as the role of epigenetic marks on active or repressed transcriptional states, and established maps of epigenetic composition in a variety of cell types in normal and cancerous tissue. However, these approaches are difficult to use to examine events occurring in heterogeneous cell populations or in uncommon cell types. This has led to the development of new techniques that permit marking of a sequence on the epigenome and improvement in the recovery yield of epigenetic material from individual cells. This has helped to determine changes in DNA, RNA, and histones, chromatin accessibility, and chromosome conformation in a variety of neoplasms. 23 , 24

In cancer, DNA hypomethylation occurs on a global scale, while hypermethylation occurs in specific genomic loci, associated with abnormal nucleosome positioning and chromatin modifications. This information has allowed epigenomic profiles to be established in different types of neoplasms. In turn, these profiles have served as the basis to identify new neoplasm subgroups. For example, in triple negative breast cancer (TNBC), 25 and in hepatocellular carcinoma, 26 DNA methylation profiles have helped to the identification of distinct subgroups with clinical relevance. Epigenetic approaches have also helped to the development of prognostic tests to assess the sensitivity of cancer cells to specific drugs. 27

Epigenetic traits could be used to characterize intratumoral heterogeneity and determine the relevance of such a heterogeneity in clonal evolution and sensitivity to drugs. However, it is clear that heterogeneity is not only determined by genetic and epigenetic diversity resulting from clonal evolution of tumor cells, but also by the various cell populations that form the tumor microenvironment (TME). 28 Consequently, the epigenome of cancer cells is continually remodeled throughout tumorigenesis, during resistance to the activity of drugs, and in metastasis. 29 This makes therapeutic action based on epigenomic profiles difficult, although significant advances in this area have been reported. 30

During carcinogenesis and tumor progression, epigenetic modifications are categorized by their mechanisms of regulation ( Figure 1A ) and the various levels of structural complexity ( Figure 1B ). In addition, the epigenome can be modified by environmental stimuli, stochastic events, and genetic variations that impact the phenotype ( Figure 1C ). 31 , 32 The molecules that take part in these mechanisms/events/variations are therapeutic targets of interest with potential impact on clinical practice. There are studies on a wide variety of epidrugs, either alone or in combination, which improve antitumor efficacy. 33 However, the problems with these drugs must not be underestimated. For a considerable number of epigenetic compounds still being under study, the main challenge is to translate in vitro efficacy of nanomolar (nM) concentrations into well-tolerated and efficient clinical use. 34 The mechanisms of action of epidrugs may not be sufficiently controlled and could lead to diversion of the therapeutic target. 35 It is known that certain epidrugs, such as valproic acid, produce unwanted epigenetic changes 36 ; thus the need for a well-established safety profile before these drugs can be used in clinical therapy. Finally, resistance to certain epidrugs is another relevant problem. 37 , 38

Epigenetics of cancer. (A) Molecular mechanisms. (B) Structural hierarchy of epigenomics. (C) Factors affecting the epigenome. Modified from Refs. 31 and 32 .

As we learn about the epigenome of specific cell populations in cancer patients, a door opens to the evaluation of sensitivity tests and the search for new molecular markers for detection, prognosis, follow-up, and/or response to treatment at various levels of molecular regulation. Likewise, the horizon expands for therapeutic alternatives in oncology with the use of epidrugs, such as pharmacoepigenomic modulators for genes and key pathways, including methylation of promoters and regulation of micro-RNAs involved in chemoresponse and immune response in cancer. 39 There is no doubt that integrated approaches identifying stable pharmagenomic and epigenomic patterns and their relation with expression profiles and genetic functions will be more and more valuable in our fight against cancer.

Cancer Stem Cells

Tumors consist of different populations of neoplastic cells and a variety of elements that form part of the TME, including stromal cells and molecules of the extracellular matrix. 40 Such intratumoral heterogeneity becomes even more complex during clonal variation of transformed cells, as well as influence the elements of the TME have on these cells throughout specific times and places. 41 To explain the origin of cancer cell heterogeneity, 2 models have been put forward. The first proposes that mutations occur at random during development of the tumor in individual neoplastic cells, and this promotes the production of various tumor populations, which acquire specific growth and survival traits that lead them to evolve according to intratumor mechanisms of natural selection. 42 The second model proposes that each tumor begins as a single cell that possess 2 functional properties: it can self-renew and it can produce several types of terminal cells. As these 2 properties are characteristics of somatic stem cells, 43 the cells have been called cancer stem cells (CSCs). 44 According to this model, tumors must have a hierarchical organization, where self-renewing stem cells produce highly proliferating progenitor cells, unable to self-renew but with a high proliferation potential. The latter, in turn, give rise to terminal cells. 45 Current evidence indicates that both models may coexist in tumor progression. In agreement with this idea, new subclones could be produced as a result of a lack of genetic stability and mutational changes, in addition to the heterogeneity derived from the initial CSC and its descendants. Thus, in each tumor, a set of neoplastic cells with different genetic and epigenetic traits may be found, which would provide different phenotypic properties. 46

The CSC concept was originally presented in a model of acute myeloid leukemia. 47 The presence of CSCs was later proved in chronic myeloid leukemia, breast cancer, tumors of the central nervous system, lung cancer, colon cancer, liver cancer, prostate cancer, pancreatic cancer, melanoma, and cancer of the head and neck, amongst others. In all of these cases, detection of CSCs was based on separation of several cell populations according to expression of specific surface markers, such as CD133, CD44, CD24, CD117, and CD15. 48 It is noteworthy that in some solid tumors, and even in some hematopoietic ones, a combination of specific markers that allow the isolation of CSCs has not been found. Interestingly, in such tumors, a high percentage of cells with the capacity to start secondary tumors has been observed; thus, the terms Tumor Initiating Cells (TIC) or Leukemia Initiating Cells (LIC) have been adopted. 46

A relevant aspect of the biology of CSCs is that, just like normal stem cells, they can self-renew. Such self-renewal guarantees the maintenance or expansion of the tumor stem cell population. Another trait CSCs share with normal stem cells is their quiescence, first described in chronic myeloid leukemia. 49 The persistence of quiescent CSCs in solid tumors has been recently described in colorectal cancer, where quiescent clones can become dominant after therapy with oxaliplatin. 50 In non-hierarchical tumors, such as melanoma, the existence of slow-cycling cells that are resistant to antimitogenic agents has also been proved. 51 Such experimental evidence supports the idea that quiescent CSCs or TICs are responsible for both tumor resistance to antineoplastic drugs and clinical relapse after initial therapeutic success.

In addition to quiescence, CSCs use other mechanisms to resist the action of chemotherapeutic drugs. One of these is their increased numbers: upon diagnosis, a high number of CSCs are observed in most analyzed tumors, making treatment unable to destroy all of them. On the other hand, CSCs have a high number of molecular pumps that expulse drugs, as well as high numbers of antiapoptotic molecules. In addition, they have very efficient mechanisms to repair DNA damage. In general, these cells show changes in a variety of signaling pathways involved in proliferation, survival, differentiation, and self-renewal. It is worth highlighting that in recent years, many of these pathways have become potential therapeutic targets in the elimination of CSCs. 52 Another aspect that is highly relevant in understanding the biological behavior of CSCs is that they require a specific site for their development within the tissue where they are found that can provide whatever is needed for their survival and growth. These sites, known as niches, are made of various cells, both tumor and non-tumor, as well as a variety of non-cellular elements (extracellular matrix [ECM], soluble cytokines, ion concentration gradients, etc.), capable of regulating the physiology of CSCs in order to promote their expansion, the invasion of adjacent tissues, and metastasis. 53

It is important to consider that although a large number of surface markers have been identified that allow us to enrich and prospectively follow tumor stem cell populations, to this day there is no combination of markers that allows us to find these populations in all tumors, and it is yet unclear if all tumors present them. In this regard, it is necessary to develop new purification strategies based on the gene expression profiles of these cells, so that tumor heterogeneity is taken into account, as it is evident that a tumor can include multiple clones of CSCs that, in spite of being functional, are genetically different, and that these clones can vary throughout space (occupying different microenvironments and niches) and time (during the progression of a range of tumor stages). Such strategies, in addition to new in vitro and in vivo assays, will allow the development of new and improved CSC elimination strategies. This will certainly have an impact on the development of more efficient therapeutic alternatives.

Invasion and Metastasis

Nearly 90% of the mortality associated with cancer is related to metastasis. 54 This consists of a cascade of events ( Figure 2 ) that begins with the local invasion of a tumor into surrounding tissues, followed by intravasation of tumor cells into the blood stream or lymphatic circulation. Extravasation of neoplastic cells in areas distant from the primary tumor then leads to the formation of one or more micrometastatic lesions which subsequently proliferate to form clinically detectable lesions. 4 The cells that are able to produce metastasis must acquire migratory characteristics, which occur by a process known as epithelial–mesenchymal transition (EMT), that is, the partial loss of epithelial characteristics and the acquirement of mesenchymal traits. 55

Invasion and metastasis cascade. Invasion and metastasis can occur early or late during tumor progression. In either case, invasion to adjacent tissues is driven by stem-like cells (cancer stem cells) that acquire the epithelial–mesenchymal transition (EMT) (1). Once they reach sites adjacent to blood vessels, tumor cells (individually or in clusters) enter the blood (2). Tumor cells in circulation can adhere to endothelium and extravasation takes place (3). Other mechanisms alternative to extravasation can exist, such as angiopelosis, in which clusters of tumor cells are internalized by the endothelium. Furthermore, at certain sites, tumor cells can obstruct microvasculature and initiate a metastatic lesion right there. Sometimes, a tumor cells that has just exit circulation goes into an MET in order to become quiescent (4). Inflammatory signals can activate quiescent metastatic cells that will proliferate and generate a clinically detectable lesion (5).

Although several of the factors involved in this process are currently known, many issues are still unsolved. For instance, it has not yet been possible to monitor in vivo the specific moment when it occurs 54 ; the microenvironmental factors of the primary tumor that promote such a transition are not known with precision; and the exact moment during tumor evolution in which one cell or a cluster of cells begin to migrate to distant areas, is also unknown. The wide range of possibilities offered by intra- and inter-tumoral heterogeneity 56 stands in the way of suggesting a generalized strategy that could resolve this complication.

It was previously believed that metastasis was only produced in late stages of tumor progression; however, recent studies indicate that EMT and metastasis can occur during the early course of the disease. In pancreatic cancer, for example, cells going through EMT are able to colonize and form metastatic lesions in the liver in the first stages of the disease. 52 , 57 Metastatic cell clusters circulating in peripheral blood (PB) are prone to generate a metastatic site, compared to individual tumor cells. 58 , 59 In this regard, novel strategies, such as the use of micro-RNAs, are being assessed in order to diminish induction of EMT. 60 It must be mentioned, however, that the metastatic process seems to be even more complex, with alternative pathways that do not involve EMT. 61 , 62

A crucial stage in the process of metastasis is the intravasation of tumor cells (alone or in clusters) towards the blood stream and/or lymphatic circulation. 63 These mechanisms are also under intensive research because blocking them could allow the control of spreading of the primary tumor. In PB or lymphatic circulation, tumor cells travel to distant parts for the potential formation of a metastatic lesion. During their journey, these cells must stand the pressure of blood flow and escape interaction with natural killer (NK) cells . 64 To avoid them, tumor cells often cover themselves with thrombocytes and also produce factors such as VEGF, angiopoietin-2, angiopoietin-4, and CCL2 that are involved in the induction of vascular permeability. 54 , 65 Neutrophils also contribute to lung metastasis in the bloodstream by secreting IL-1β and metalloproteases to facilitate extravasation of tumor cells. 64

The next step in the process of metastasis is extravasation, for which tumor cells, alone or in clusters, can use various mechanisms, including a recently described process known as angiopellosis that involves restructuring the endothelial barrier to internalize one or several cells into a tissue. 66 The study of leukocyte extravasation has contributed to a more detailed knowledge of this process, in such a way that some of the proposed strategies to avoid extravasation include the use of integrin inhibitors, molecules that are vital for rolling, adhesion, and extravasation of tumor cells. 67 , 68 Another strategy that has therapeutic potential is the use of antibodies that strengthen vascular integrity to obstruct transendothelial migration of tumor cells and aid in their destruction in PB. 69

Following extravasation, tumor cells can return to an epithelial phenotype, a process known as mesenchymal–epithelial transition and may remain inactive for several years. They do this by competing for specialized niches, like those in the bone marrow, brain, and intestinal mucosa, which provide signals through the Notch and Wnt pathways. 70 Through the action of the Wnt pathway, tumor cells enter a slow state of the cell cycle and induce the expression of molecules that inhibit the cytotoxic function of NK cells. 71 The extravasated tumor cell that is in a quiescent state must comply with 2 traits typical of stem cells: they must have the capacity to self-renew and to generate all of the cells that form the secondary tumor.

There are still several questions regarding the metastatic process. One of the persisting debates at present is if EMT is essential for metastasis or if it plays a more important role in chemoresistance. 61 , 62 It is equally important to know if there is a pattern in each tumor for the production of cells with the capacity to carry out EMT. In order to control metastasis, it is fundamental to know what triggers acquisition of the migratory phenotype and the intrinsic factors determining this transition. Furthermore, it is essential to know if mutations associated with the primary tumor or the variety of epigenetic changes are involved in this process. 55 It is clear that metastatic cells have affinity for certain tissues, depending on the nature of the primary tumor (seed and soil hypothesis). This may be caused by factors such as the location and the direction of the bloodstream or lymphatic fluid, but also by conditioning of premetastatic niches at a distance (due to the large number of soluble factors secreted by the tumor and the recruitment of cells of the immune system to those sites). 72 We have yet to identify and characterize all of the elements that participate in this process. Deciphering them will be of upmost importance from a therapeutic point of view.

Epidemiology of Cancer

Cancer is the second cause of death worldwide; today one of every 6 deaths is due to a type of cancer. According to the International Agency for Research on Cancer (IARC), in 2020 there were approximately 19.3 million new cases of cancer, and 10 million deaths by this disease, 6 while 23.8 million cases and 13.0 million deaths are projected to occur by 2030. 73 In this regard, it is clear the increasing role that environmental factors—including environmental pollutants and processed food—play as cancer inducers and promoters. 74 The types of cancer that produce the greatest numbers of cases and deaths worldwide are indicated in Table 1 . 6

Total Numbers of Cancer Cases and Deaths Worldwide in 2020 by Cancer Type (According to the Global Cancer Observatory, IARC).

Data presented on this table were obtained from Ref. 6.

As shown in Figure 3 , lung, breast, prostate, and colorectal cancer are the most common throughout the world, and they are mostly concentrated in countries of high to very high human development index (HDI). Although breast, prostate, and colorectal cancer have a high incidence, the number of deaths they cause is proportionally low, mostly reflecting the great progress made in their control. However, these data also reveal the types of cancer that require further effort in prevention, precise early detection avoiding overdiagnosis, and efficient treatment. This is the case of liver, lung, esophageal, and pancreatic cancer, where the difference between the number of cases and deaths is smaller ( Figure 3B ). Social and economic transition in several countries has had an impact on reducing the incidence of neoplasms associated with infection and simultaneously produced an increase in the types related to reproductive, dietary, and hormonal factors. 75

Incidence and mortality for some types of cancer in the world. (A) Estimated number of cases and deaths in 2020 for the most frequent cancer types worldwide. (B) Incidence and mortality rates, normalized according to age, for the most frequent cancer types in countries with very high/& high (VH&H; blue) and/low and middle (L&M; red) Human Development Index (HDI). Data include both genders and all ages. Data according to https://gco.iarc.fr/today , as of June 10, 2021.

In the past 3 decades, cancer mortality rates have fallen in high HDI countries, with the exception of pancreatic cancer, and lung cancer in women. Nevertheless, changes in the incidence of cancer do not show the same consistency, possibly due to variables such as the possibility of early detection, exposure to risk factors, or genetic predisposition. 76 , 77 Countries such as Australia, Canada, Denmark, Ireland, New Zealand, Norway, and the United Kingdom have reported a reduction in incidence and mortality in cancer of the stomach, colon, lung, and ovary, as well as an increase in survival. 78 Changes in modifiable risk factors, such as the use of tobacco, have played an important role in prevention. In this respect, it has been estimated that decline in tobacco use can explain between 35% and 45% of the reduction in cancer mortality rates, 79 while the fall in incidence and mortality due to stomach cancer can be attributed partly to the control of Helicobacter pylori infection. 80 Another key factor in the fall of mortality rates in developed countries has been an increase in early detection as a result of screening programs, as in breast and prostate cancer, which have had their mortality rates decreased dramatically in spite of an increase in their incidence. 76

Another important improvement observed in recent decades is the increase in survival rates, particularly in high HDI countries. In the USA, for example, survival rates for patients with prostate cancer at 5 years after initial diagnosis was 28% during 1947–1951; 69% during 1975–1977, and 100% during 2003–2009. Something similar occurred with breast cancer, with a 5-year survival rate of 54% in 1947–1951, 75% in 1975–1977, and 90% in 2003–2009. 81 In the CONCORD 3 version, age-standardize 5-year survival for patients with breast cancer in the USA during 2010–2014 was 90%, and 97% for prostate cancer patients. 82 Importantly, even among high HDI countries, significant differences have been identified in survival rates, being stage of disease at diagnosis, time for access to effective treatment, and comorbidities, the main factors influencing survival in these nations. 78 Unfortunately, survival rates in low HDI countries are significantly lower due to several factors, including lack of information, deficient screening and early detection programs, limited access to treatment, and suboptimal cancer registration. 82 It should be noted that in countries with low to middle HDI, neoplasms with the greatest incidence are those affecting women (breast and cervical cancer), which reflects not only a problem with access to health services, but also a serious inequality issue that involves social, cultural, and even religious obstacles. 83

Up to 42% of incident cases and 47% of deaths by cancer in the USA are due to potentially modifiable risk factors such as use of tobacco, physical activity, diet, and infection. 84 It has been calculated that 2.4 million deaths by cancer, mostly of the lung, can be attributed to tobacco. 73 In 2020, the incidence rate of lung cancer in Western Africa was 2.2, whereas in Polynesia and Eastern Asia was 37.3 and 34.4, respectively. 6 In contrast, the global burden of cancer associated with infection was 15.4%, but in Sub-Saharan Africa it was 30%. 85 Likewise, the incidence of cervical cancer in Eastern Africa was 40.1, in contrast with the USA and Canada that have a rate of 6.2. This makes it clear that one of the challenges we face is the reduction of the risk factors that are potentially modifiable and associated with specific types of cancer.

Improvement of survival rates and its disparities worldwide are also important challenges. Five-year survival for breast cancer—diagnosed during 2010-2014— in the USA, for example, was 90%, whereas in countries like South Africa it was 40%. 82 Childhood leukemia in the USA and several European countries shows a 5-year survival of 90%, while in Latin-American countries it is 50–76%. 86 Interestingly, there are neoplasms, such as pancreatic cancer, for which there has been no significant increase in survival, which remains low (5–15%) both in developed and developing countries. 82

Although data reported on global incidence and mortality gives a general overview on the epidemiology of cancer, it is important to note that there are great differences in coverage of cancer registries worldwide. To date, only 1 out of every 3 countries reports high quality data on the incidence of cancer. 87 For the past 50 years, the IARC has supported population-based cancer registries; however, more than one-third of the countries belonging to the WHO, mainly countries of low and middle income (LMIC), have no data on more than half of the 18 indicators of sustainable development goals. 88 High quality cancer registries only cover 4% of the population in Africa, 8% in Asia, and 7% in Latin America, contrasting with 83% in the USA and Canada, and 33% in Europe. 89 In response to this situation, the Global Initiative for Cancer Registry Development was created in 2012 to generate improved infrastructure to permit greater coverage and better quality registries, especially in countries with low and middle HDI. 88 It is expected that initiatives of this sort in the coming years will allow more and better information to guide strategies for the control of cancer worldwide, especially in developing regions. This will enable survival to be measured over longer periods of time (10, 15, or 20 years), as an effective measure in the control of cancer. The WHO has established as a target for 2025 to reduce deaths by cancer and other non-transmissible diseases by 25% in the population between the ages of 30–69; such an effort requires not only effective prevention measures to reduce incidence, but also more efficient health systems to diminish mortality and increase survival. At the moment, it is an even greater challenge because of the effects of the COVID-19 pandemic which has negatively impacted cancer prevention and health services. 90

Oncologic Treatments

A general perspective.

At the beginning of the 20th century, cancer treatment, specifically treatment of solid tumors, was based fundamentally on surgical resection of tumors, which together with other methods for local control, such as cauterization, had been used since ancient times. 91 At that time, there was an ongoing burst of clinical observations along with interventions sustained on fundamental knowledge about physics, chemistry, and biology. In the final years of the 19 th century and the first half of the 20th, these technological developments gave rise to radiotherapy, hormone therapy, and chemotherapy. 92 - 94 Simultaneously, immunotherapy was also developed, although usually on a smaller scale, in light of the overwhelming progress of chemotherapy and radiotherapy. 95

Thus began the development and expansion of disciplines based on these approaches (surgery, radiotherapy, chemotherapy, hormone therapy, and immunotherapy), with their application evolving ever more rapidly up to their current uses. Today, there is a wide range of therapeutic tools for the care of cancer patients. These include elements that emerged empirically, arising from observations of their effects in various medical fields, as well as drugs that were designed to block processes and pathways that form part of the physiopathology of one or more neoplasms according to knowledge of specific molecular alterations. A classic example of the first sort of tool is mustard gas, originally used as a weapon in war, 96 but when applied for medical purposes, marked the beginning of the use of chemicals in the treatment of malignant neoplasms, that is, chemotherapy. 94 A clear example of the second case is imatinib, designed specifically to selectively inhibit a molecular alteration in chronic myeloid leukemia: the Bcr-Abl oncoprotein. 97

It is on this foundation that today the 5 areas mentioned previously coexist and complement one another. The general framework that motivates this amalgam and guides its development is precision medicine, founded on the interaction of basic and clinical science. In the forecasts for development in each of these fields, surgery is expected to continue to be the fundamental approach for primary tumors in the foreseeable future, as well as when neoplastic disease in the patient is limited, or can be limited by applying systemic or regional elements, before and/or after surgical resection, and it can be reasonably anticipated for the patient to have a significant period free from disease or even to be cured. With regards to technology, intensive exploration of robotic surgery is contemplated. 98

The technological possibilities for radiotherapy have progressed in such a way that it is now possible to radiate neoplastic tissue with an extraordinary level of precision, and therefore avoid damage to healthy tissue. 99 This allows administration of large doses of ionizing radiation in one or a few fractions, what is known as “radiosurgery.” The greatest challenges to the efficacy of this approach are related to radio-resistance in certain neoplasms. Most efforts regarding research in this field are concentrated on understanding the underlying biological mechanisms of the phenomenon and their potential control through radiosensitizers. 100

“Traditional” chemotherapy, based on the use of compounds obtained from plants and other natural products, acting in a non-specific manner on both neoplastic and healthy tissues with a high proliferation rate, continues to prevail. 101 The family of chemotherapeutic drugs currently includes alkylating agents, antimetabolites, anti-topoisomerase agents, and anti-microtubules. Within the pharmacologic perspective, the objective is to attain a high concentration or activity of such molecules in specific tissues while avoiding their accumulation in others, in order to achieve an increase in effectiveness and a reduction in toxicity. This has been possible with the use of viral vectors, for example, that are able to limit their replication in neoplastic tissues, and activate prodrugs of normally nonspecific agents, like cyclophosphamide, exclusively in those specific areas. 102 More broadly, chemotherapy also includes a subgroup of substances, known as molecular targeted therapy, that affect processes in a more direct and specific manner, which will be mentioned later.

There is no doubt that immunotherapy—to be explored next—is one of the therapeutic fields where development has been greatest in recent decades and one that has produced enormous expectation in cancer treatment. 103 Likewise, cell therapy, based on the use of immune cells or stem cells, has come to complement the oncologic therapeutic arsenal. 43 Each and every one of the therapeutic fields that have arisen in oncology to this day continue to prevail and evolve. Interestingly, the foreseeable future for the development of cancer treatment contemplates these approaches in a joint and complementary manner, within the general framework of precision medicine, 104 and sustained by knowledge of the biological mechanisms involved in the appearance and progression of neoplasms. 105 , 106

Immunotherapy

Stimulating the immune system to treat cancer patients has been a historical objective in the field of oncology. Since the early work of William Coley 107 to the achievements reached at the end of the 20 th century, scientific findings and technological developments paved the way to searching for new immunotherapeutic strategies. Recombinant DNA technology allowed the synthesis of cytokines, such as interferon-alpha (IFN-α) and interleukin 2 (IL-2), which were authorized by the US Food and Drug Administration (FDA) for the treatment of hairy cell leukemia in 1986, 108 as well as kidney cancer and metastatic melanoma in 1992 and 1998, respectively. 109

The first therapeutic vaccine against cancer, based on the use of autologous dendritic cells (DCs), was approved by the FDA against prostate cancer in 2010. However, progress in the field of immunotherapy against cancer was stalled in the first decade of the present century, mostly due to failure of several vaccines in clinical trials. In many cases, application of these vaccines was detained by the complexity and cost involved in their production. Nevertheless, with the coming of the concept of immune checkpoint control, and the demonstration of the relevance of molecules such as cytotoxic T-lymphocyte antigen 4 (CTLA-4), and programmed cell death molecule-1 (PD-1), immunotherapy against cancer recovered its global relevance. In 2011, the monoclonal antibody (mAb) ipilimumab, specific to the CTLA-4 molecule, was the first checkpoint inhibitor (CPI) approved for the treatment of advanced melanoma. 110 Later, inhibitory mAbs for PD-1, or for the PD-1 ligand (PD-L1), 111 as well as the production of T cells with chimeric receptors for antigen recognition (CAR-T), 112 which have been approved to treat various types of cancer, including melanoma, non-small cell lung cancer (NSCLC), head and neck cancer, bladder cancer, renal cell carcinoma (RCC), and hepatocellular carcinoma, among others, have changed the paradigm of cancer treatment.

In spite of the current use of anti-CTLA-4 and anti-PD-L1 mAbs, only a subgroup of patients has responded favorably to these CPIs, and the number of patients achieving clinical benefit is still small. It has been estimated that more than 70% of patients with solid tumors do not respond to CPI immunotherapy because either they show primary resistance, or after responding favorably, develop resistance to treatment. 113 In this regard, it is important to mention that in recent years very important steps have been taken to identify the intrinsic and extrinsic mechanisms that mediate resistance to CPI immunotherapy. 114 Intrinsic mechanisms include changes in the antitumor immune response pathways, such as faulty processing and presentation of antigens by APCs, activation of T cells for tumor cell destruction, and changes in tumor cells that lead to an immunosuppressive TME. Extrinsic factors include the presence of immunosuppressive cells in the local TME, such as regulatory T cells, myeloid-derived suppressor cells (MDSC), mesenchymal stem/stromal cells (MSCs), and type 2 macrophages (M2), in addition to immunosuppressive cytokines.

On the other hand, classification of solid tumors as “hot,” “cold,” or “excluded,” depending on T cell infiltrates and the contact of such infiltrates with tumor cells, as well as those that present high tumor mutation burden (TMB), have redirected immunotherapy towards 3 main strategies 115 ( Table 2 ): (1) Making T-cell antitumor response more effective, using checkpoint inhibitors complementary to anti-CTLA-4 and anti-PD-L1, such as LAG3, Tim-3, and TIGT, as well as using CAR-T cells against tumor antigens. (2) Activating tumor-associated myeloid cells including monocytes, granulocytes, macrophages, and DC lineages, found at several frequencies within human solid tumors. (3) Regulating the biochemical pathways in TME that produce high concentrations of immunosuppressive molecules, such as kynurenine, a product of tryptophan metabolism, through the activity of indoleamine 2,3 dioxygenase; or adenosine, a product of ATP hydrolysis by the activity of the enzyme 5’nucleotidase (CD73). 116

Current Strategies to Stimulate the Immune Response for Antitumor Immunotherapy.

Abbreviations: TME, tumor microenvironment; IL, interleukin; TNF, Tumor Necrosis Factor; TNFR, TNF-receptor; CD137, receptor–co-stimulator of the TNFR family; OX40, member number 4 of the TNFR superfamily; CD27/CD70, member of the TNFR superfamily; CD40/CD40L, antigen-presenting cells (APC) co-stimulator and its ligand; GM-CSF, granulocyte-macrophage colony-stimulating factor; IFN, interferon; STING, IFN genes-stimulator; RIG-I, retinoic acid inducible gene-I; MDA5, melanoma differentiation-associated protein 5; CDN, cyclic dinucleotide; ATP, adenosine triphosphate; HMGB1, high mobility group B1 protein; TLR, Toll-like receptor; HVEM, Herpes virus entry mediator; GITR, glucocorticoid-induced TNFR family-related gene; CTLA4, cytotoxic T lymphocyte antigen 4; PD-L1, programmed death ligand-1; TIGIT, T-cell immunoreceptor with immunoglobulin and tyrosine-based inhibition motives; CSF1/CSF1R, colony-stimulating factor-1 and its receptor; CCR2, Type 2 chemokine receptor; PI3Kγ, Phosphoinositide 3-Kinase γ; CXCL/CCL, chemokine ligands; LFA1, lymphocyte function-associated antigen 1; ICAM1, intercellular adhesion molecule 1; VEGF, vascular endothelial growth factor; IDO, indolamine 2,3-dioxigenase; TGF, transforming growth factor; LAG-3, lymphocyte-activation gene 3 protein; TIM-3, T-cell immunoglobulin and mucin-domain containing-3; CD73, 5´nucleotidase; ARs, adenosine receptors; Selectins, cell adhesion molecules; CAR-T, chimeric antigen receptor T cell; TCR-T, T-cell receptor engineered T cell.

Apart from the problems associated with its efficacy (only a small group of patients respond to it), immunotherapy faces several challenges related to its safety. In other words, immunotherapy can induce adverse events in patients, such as autoimmunity, where healthy tissues are attacked, or cytokine release syndrome and vascular leak syndrome, as observed with the use of IL-2, both of which lead to serious hypotension, fever, renal failure, and other adverse events that are potentially lethal. The main challenges to be faced by immunotherapy in the future will require the combined efforts of basic and clinical scientists, with the objective of accelerating the understanding of the complex interactions between cancer and the immune system, and improve treatment options for patients. Better comprehension of immune phenotypes in tumors, beyond the state of PD-L1 and TME, will be relevant to increase immunotherapy efficacy. In this context, the identification of precise tumor antigenicity biomarkers by means of new technologies, such as complete genome sequencing, single cell sequencing, and epigenetic analysis to identify sites or subclones typical in drug resistance, as well as activation, traffic and infiltration of effector cells of the immune response, and regulation of TME mechanisms, may help define patient populations that are good candidates for specific therapies and therapeutic combinations. 117 , 118 Likewise, the use of agents that can induce specific activation and modulation of the response of T cells in tumor tissue, will help improve efficacy and safety profiles that can lead to better clinical results.

Molecular Targeted Therapy

For over 30 years, and based on the progress in our knowledge of tumor biology and its mechanisms, there has been a search for therapeutic alternatives that would allow spread and growth of tumors to be slowed down by blocking specific molecules. This approach is known as molecular targeted therapy. 119 Among the elements generally used as molecular targets there are transcription factors, cytokines, membrane receptors, molecules involved in a variety of signaling pathways, apoptosis modulators, promoters of angiogenesis, and cell cycle regulators. 120

Imatinib, a tyrosine kinase inhibitor for the treatment of chronic myeloid leukemia, became the first targeted therapy in the final years of the 1990s. 97 From then on, new drugs have been developed by design, and today more than 60 targeted therapies have been approved by the FDA for the treatment of a variety of cancers ( Table 3 ). 121 This has had a significant impact on progression-free survival and global survival in neoplasms such as non-small cell lung cancer, breast cancer, renal cancer, and melanoma.

FDA Approved Molecular Targeted Therapies for the Treatment of Solid Tumors.

Abbreviations: mAb, monoclonal antibody; ALK, anaplastic lymphoma kinase; CDK, cyclin-dependent kinase; CTLA-4, cytotoxic lymphocyte antigen-4; EGFR, epidermal growth factor receptor; FGFR, fibroblast growth factor receptor; GIST, gastrointestinal stroma tumor; mTOR, target of rapamycine in mammal cells; NSCLC, non-small cell lung carcinoma; PARP, poli (ADP-ribose) polimerase; PD-1, programmed death protein-1; PDGFR, platelet-derived growth factor receptor; PD-L1, programmed death ligand-1; ER, estrogen receptor; PR, progesterone receptor; TKR, tyrosine kinase receptors; SERM, selective estrogen receptor modulator; TKI, tyrosine kinase inhibitor; VEGFR, vascular endothelial growth factor receptor. Modified from Ref. [ 127 ].

Most drugs classified as targeted therapies form part of 2 large groups: small molecules and mAbs. The former are defined as compounds of low molecular weight (<900 Daltons) that act upon entering the cell. 120 Targets of these compounds are cell cycle regulatory proteins, proapoptotic proteins, or DNA repair proteins. These drugs are indicated based on histological diagnosis, as well as molecular tests. In this group there are multi-kinase inhibitors (RTKs) and tyrosine kinase inhibitors (TKIs), like sunitinib, sorafenib, and imatinib; cyclin-dependent kinase (CDK) inhibitors, such as palbociclib, ribociclib and abemaciclib; poli (ADP-ribose) polimerase inhibitors (PARPs), like olaparib and talazoparib; and selective small-molecule inhibitors, like ALK and ROS1. 122

As for mAbs, they are protein molecules that act on membrane receptors or extracellular proteins by interrupting the interaction between ligands and receptors, in such a way that they reduce cell replication and induce cytostasis. Among the most widely used mAbs in oncology we have: trastuzumab, a drug directed against the receptor for human epidermal growth factor-2 (HER2), which is overexpressed in a subgroup of patients with breast and gastric cancer; and bevacizumab, that blocks vascular endothelial growth factor and is used in patients with colorectal cancer, cervical cancer, and ovarian cancer. Other mAbs approved by the FDA include pembolizumab, atezolizumab, nivolumab, avelumab, ipilimumab, durvalumab, and cemiplimab. These drugs require expression of response biomarkers, such as PD-1 and PD-L1, and must also have several resistance biomarkers, such as the expression of EGFR, the loss of PTEN, and alterations in beta-catenin. 123

Because cancer is such a diverse disease, it is fundamental to have precise diagnostic methods that allow us to identify the most adequate therapy. Currently, basic immunohistochemistry is complemented with neoplastic molecular profiles to determine a more accurate diagnosis, and it is probable that in the near future cancer treatments will be based exclusively on molecular profiles. In this regard, it is worth mentioning that the use of targeted therapy depends on the existence of specific biomarkers that indicate if the patient will be susceptible to the effects of the drug or not. Thus, the importance of underlining that not all patients are susceptible to receive targeted therapy. In certain neoplasms, therapeutic targets are expressed in less than 5% of the diagnosed population, hindering a more extended use of certain drugs.

The identification of biomarkers and the use of new generation sequencing on tumor cells has shown predictive and prognostic relevance. Likewise, mutation analysis has allowed monitoring of tumor clone evolution, providing information on changes in canonic gene sequences, such as TP53, GATA3, PIK3CA, AKT1, and ERBB2; infrequent somatic mutations developed after primary treatments, like SWI-SNF and JAK2-STAT3; or acquired drug resistance mutations such as ESR1. 124 The study of mutations is vital; in fact, many of them already have specific therapeutic indications, which have helped select adequate treatments. 125

There is no doubt that molecular targeted therapy is one of the main pillars of precision medicine. However, it faces significant problems that often hinder obtaining better results. Among these, there is intratumor heterogeneity and differences between the primary tumor and metastatic sites, as well as intrinsic and acquired resistance to these therapies, the mechanisms of which include the presence of heterogeneous subclones, DNA hypermethylation, histone acetylation, and interruption of mRNA degradation and translation processes. 126 Nonetheless, beyond the obstacles facing molecular targeted therapy from a biological and methodological point of view, in the real world, access to genomic testing and specific drugs continues to be an enormous limitation, in such a way that strategies must be designed in the future for precision medicine to be possible on a global scale.

Cell Therapy

Another improvement in cancer treatment is the use of cell therapy, that is, the use of specific cells as therapeutic agents. This clinical procedure has 2 modalities: the first consists of replacing and regenerating functional cells in a specific tissue by means of stem/progenitor cells of a certain kind, 43 while the second uses immune cells as effectors to eliminate malignant cells. 127

Regarding the first type, we must emphasize the development of cell therapy based on hematopoietic stem and progenitor cells. 128 For over 50 years, hematopoietic cell transplants have been used to treat a variety of hematologic neoplasms (different forms of leukemia and lymphoma). Today, it is one of the most successful examples of cell therapy, including innovative modalities, such as haploidentical transplants, 129 as well as application of stem cells expanded ex vivo . 130 There are also therapies that have used immature cells that form part of the TME, such as MSCs. The replication potential and cytokine secretion capacity of these cells make them an excellent option for this type of treatment. 131 Neural stem cells can also be manipulated to produce and secrete apoptotic factors, and when these cells are incorporated into primary neural tumors, they cause a certain degree of regression. They can even be transfected with genes that encode for oncolytic enzymes capable of inducing regression of glioblastomas. 132

With respect to cell therapy using immune cells, several research groups have manipulated cells associated with tumors to make them effector cells and thus improve the efficacy and specificity of the antitumor treatment. PB leckocytes cultured in the presence of IL-2 to obtain activated lymphocytes, in combination with IL-2 administration, have been used in antitumor clinical protocols. Similarly, infiltrating lymphocytes from tumors with antitumor activity have been used and can be expanded ex vivo with IL-2. These lymphocyte populations have been used in immunomodulatory therapies in melanoma, and pancreatic and kidney tumors, producing a favorable response in treated patients. 133 NK cells and macrophages have also been used in immunotherapy, although with limited results. 134 , 135

One of the cell therapies with better projection today is the use of CAR-T cells. This strategy combines 2 forms of advanced therapy: cell therapy and gene therapy. It involves the extraction of T cells from the cancer patient, which are genetically modified in vitro to express cell surface receptors that will recognize antigens on the surface of tumor cells. The modified T cells are then reintroduced in the patient to aid in an exacerbated immune response that leads to eradication of the tumor cells ( Figure 4 ). Therapy with CAR-T cells has been used successfully in the treatment of some types of leukemia, lymphoma, and myeloma, producing complete responses in patients. 136

CAR-T cell therapy. (A) T lymphocytes obtained from cancer patients are genetically manipulated to produce CAR-T cells that recognize tumor cells in a very specific manner. (B) Interaction between CAR molecule and tumor antigen. CAR molecule is a receptor that results from the fusion between single-chain variable fragments (scFv) from a monoclonal antibody and one or more intracellular signaling domains from the T-cell receptor. CD3ζ, CD28 and 4-1BB correspond to signaling domains on the CAR molecule.

Undoubtedly, CAR-T cell therapy has been truly efficient in the treatment of various types of neoplasms. However, this therapeutic strategy can also have serious side effects, such as release of cytokines into the bloodstream, which can cause different symptoms, from high fever to multiorgan failure, and even neurotoxicity, leading to cerebral edema in many cases. 137 Adequate control of these side effects is an important medical challenge. Several research groups are trying to improve CAR-T cell therapy through various approaches, including production of CAR-T cells directed against a wider variety of tumor cell-specific antigens that are able to attack different types of tumors, and the identification of more efficient types of T lymphocytes. Furthermore, producing CAR-T cells from a single donor that may be used in the treatment of several patients would reduce the cost of this sort of personalized cell therapy. 136

Achieving wider use of cell therapy in oncologic diseases is an important challenge that requires solving various issues. 138 One is intratumor cell heterogeneity, including malignant subclones and the various components of the TME, which results in a wide profile of membrane protein expression that complicates finding an ideal tumor antigen that allows specific identification (and elimination) of malignant cells. Likewise, structural organization of the TME challenges the use of cell therapy, as administration of cell vehicles capable of recognizing malignant cells might not be able to infiltrate the tumor. This results from low expression of chemokines in tumors and the presence of a dense fibrotic matrix that compacts the inner tumor mass and avoids antitumor cells from infiltrating and finding malignant target cells.

Further Challenges in the 21st Century

Beyond the challenges regarding oncologic biomedical research, the 21 st century is facing important issues that must be solved as soon as possible if we truly wish to gain significant ground in our fight against cancer. Three of the most important have to do with prevention, early diagnosis, and access to oncologic medication and treatment.

Prevention and Early Diagnosis

Prevention is the most cost-effective strategy in the long term, both in low and high HDI nations. Data from countries like the USA indicate that between 40-50% of all types of cancer are preventable through potentially modifiable factors (primary prevention), such as use of tobacco and alcohol, diet, physical activity, exposure to ionizing radiation, as well as prevention of infection through access to vaccination, and by reducing exposure to environmental pollutants, such as pesticides, diesel exhaust particles, solvents, etc. 74 , 84 Screening, on the other hand, has shown great effectiveness as secondary prevention. Once population-based screening programs are implemented, there is generally an initial increase in incidence; however, in the long term, a significant reduction occurs not only in incidence rates, but also in mortality rates due to detection of early lesions and timely and adequate treatment.

A good example is colon cancer. There are several options for colon cancer screening, such as detection of fecal occult blood, fecal immunohistochemistry, flexible sigmoidoscopy, and colonoscopy, 139 , 140 which identify precursor lesions (polyp adenomas) and allow their removal. Such screening has allowed us to observe 3 patterns of incidence and mortality for colon cancer between the years 2000 and 2010: on one hand, an increase in incidence and mortality in countries with low to middle HDI, mainly countries in Asia, South America, and Eastern Europe; on the other hand, an increase in incidence and a fall in mortality in countries with very high HDI, such as Canada, the United Kingdom, Denmark, and Singapore; and finally a fall in incidence and mortality in countries like the USA, Japan, and France. The situation in South America and Asia seems to reflect limitations in medical infrastructure and a lack of access to early detection, 141 while the patterns observed in developed countries reveal the success, even if it may be partial, of that which can be achieved by well-structured prevention programs.

Another example of success, but also of strong contrast, is cervical cancer. The discovery of the human papilloma virus (HPV) as the causal agent of cervical cancer brought about the development of vaccines and tests to detect oncogenic genotypes, which modified screening recommendations and guidelines, and allowed several developed countries to include the HPV vaccine in their national vaccination programs. Nevertheless, the outlook is quite different in other areas of the world. Eighty percent of the deaths by cervical cancer reported in 2018 occurred in low-income nations. This reveals the urgency of guaranteeing access to primary and secondary prevention (vaccination and screening, respectively) in these countries, or else it will continue to be a serious public health problem in spite of its preventability.

Screening programs for other neoplasms, such as breast, prostate, lung, and thyroid cancer have shown outlooks that differ from those just described, because, among other reasons, these neoplasms are highly diverse both biologically and clinically. Another relevant issue is the overdiagnosis of these neoplasms, that is, the diagnosis of disease that would not cause symptoms or death in the patient. 142 It has been calculated that 25% of breast cancer (determined by mammogram), 50–60% of prostate cancer (determined by PSA), and 13–25% of lung cancer (determined by CT) are overdiagnosed. 142 Thus, it is necessary to improve the sensitivity and specificity of screening tests. In this respect, knowledge provided by the biology of cancer and “omic” sciences offers a great opportunity to improve screening and prevention strategies. All of the above shows that prevention and early diagnosis are the foundations in the fight against cancer, and it is essential to continue to implement broader screening programs and better detection methods.

Global Equity in Oncologic Treatment

Progress in cancer treatment has considerably increased the number of cancer survivors. Nevertheless, this tendency is evident only in countries with a very solid economy. Indeed, during the past 30 years, cancer mortality rates have increased 30% worldwide. 143 Global studies indicate that close to 70% of cancer deaths in the world occur in nations of low to middle income. But even in high-income countries, there are sectors of society that are more vulnerable and have less access to cancer treatments. 144 Cancer continues to be a disease of great social inequality.

In Europe, the differences in access to cancer treatment are highly marked. These treatments are more accessible in Western Europe than in its Eastern counterpart. 145 Furthermore, highly noticeable differences between high-income countries have been detected in the cost of cancer drugs. 146 It is interesting to note that in many of these cases, treatment is too costly and the clinical benefit only marginal. Thus, the importance of these problems being approached by competent national, regional, and global authorities, because if these new drugs and therapeutic programs are not accessible to the majority, progress in biomedical, clinical and epidemiological research will have a limited impact in our fight against cancer. We must not forget that health is a universal right, from which low HDI countries must not be excluded, nor vulnerable populations in nations with high HDI. The participation of a well-informed society will also be fundamental to achieve a global impact, as today we must fight not only against the disease, but also against movements and ideas (such as the anti-vaccine movement and the so-called miracle therapies) that can block the medical battle against cancer.

Final Comments

From the second half of the 20th century to the present day, progress in our knowledge about the origin and development of cancer has been extraordinary. We now understand cancer in detail in genomic, molecular, cellular, and physiological terms, and this knowledge has had a significant impact in the clinic. There is no doubt that a patient who is diagnosed today with a type of cancer has a better prospect than a patient diagnosed 20 or 50 years ago. However, we are still far from winning the war against cancer. The challenges are still numerous. For this reason, oncologic biomedical research must be a worldwide priority. Likewise, one of the fundamental challenges for the coming decades must be to reduce unequal access to health services in areas of low- to middle income, and in populations that are especially vulnerable, as well as continue improving prevention programs, including public health programs to reduce exposure to environmental chemicals and improve diet and physical activity in the general population. 74 , 84 Fostering research and incorporation of new technological resources, particularly in less privileged nations, will play a key role in our global fight against cancer.

Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding: The author(s) received no financial support for the research, authorship, and/or publication of this article.

Hector Mayani https://orcid.org/0000-0002-2483-3782

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Essay on Cancer Prevention | Types | Diseases | Biology

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Read this essay to examine various agents that have the greatest impact in decreasing cancer incidence and deaths.

1. Essay on Cancer Prevention: (Around 650 Words)

Not Smoking is the most Effective Way to Reduce the Risk of Developing a Fatal Cancer :

Cigarette smoking is the number one cause of preventable cancer deaths. Tobacco smoke contains dozens of carcinogenic chemicals. If people did not smoke ciga­rettes, roughly one of every three cancer deaths would be prevented.

Progress has been made over the past several decades in lowering smoking rates in the United States, but these gains have been offset by a growing epidemic of cigarette smoking elsewhere in the world. Even in the United States, close to 50 million people smoke cigarettes and smoking is the leading cause of preventable death, killing more people than AIDS, car accidents, murder, alcohol, illegal drugs, and suicides combined.

Figure 1 illustrates the trends in smoking rates in the United States since 1900. In the first half of the twentieth century, cigarette consumption increased from a yearly average of several dozen cigarettes per person in 1900 to more than 4000 per person in 1963. Then in 1964, the U.S. government published the first Surgeon General’s Report on Smoking and Health.

Based on an analysis of more than 7000 scien­tific investigations involving a variety of experimental and epidemiological approaches, the report concluded that cigarette smoking causes lung cancer. At that point, smoking rates in the United States stopped growing and slowly began to decline.

Improved education has played an important role in stimulating this decline. In general, smoking behavior is inversely related to a person’s overall level of education: Statistics show that roughly 30% of those without a high school diploma smoke cigarettes compared with about 10% of college graduates (Figure 2).

A variety of governmental actions have also contributed to the decline in smoking rates. Included in this category are laws requiring warning labels on cigarette packages, which inform people about the health hazards of tobacco, and high taxation of tobacco products and restrictions on smoking in public places, both of which tend to discourage smoking behaviors.

One obstacle to further progress is the difficulty that people encounter when they try to quit smoking. About half of all adult smokers express a desire to stop smoking and make at least one attempt to quit annually, yet fewer than 15% can refrain from smoking for more than 30 days.

The addictive power of the nicotine in tobacco is clearly a major impediment. Although some people overcome their nicotine addiction and quit smoking through sheer willpower, success rates are improved by supportive social arrangements, such as smoking cessation clinics, combined with drug treatments for nicotine dependence (e.g., nicotine patches or sprays and even antidepressants).

The motivation to quit might also be enhanced by better education regarding the dramatic drop in cancer risk that occurs after people stop smoking. In the 20-year period after quitting, lung cancer rates drop about tenfold to reach a level that is only slightly higher than that observed in individuals who have never smoked at all (Figure 3).

Moreover, the reduction in risk is not restricted to lung cancer. Smoking cessation is also associated with a decreased risk for cancers of the mouth, pharynx, larynx, esophagus, stomach, pancreas, uterine cervix, kidney, bladder, and colon, as well as leukemias.

Most tobacco-related cancers are linked to cigarette use, but other tobacco products—such as cigars, pipes, and smokeless tobacco—also cause cancer. Smoking cigars or a pipe triggers most of the same cancers as cigarettes, although the risk of lung cancer is less than with cigarettes because cigar or pipe smoke is not inhaled as deeply into the lungs.

Secondhand smoke can also cause cancer, although the risk is small compared with that associated with the direct use of tobacco products. Smoke is not even required for tobacco to exert its carcinogenic effects. Smokeless tobacco, which is chewed rather than smoked, causes numerous cancers of the mouth and throat, as well as some in the esophagus, stomach, and pancreas.

2. Essay on Cancer Prevention: (Around 300 Words)

Alcohol Consumption is Associated with Cancer Risks, but also Cardiovascular Benefits when used in Moderate Amounts :

Alcohol consumption is associated with an increased risk for several types of cancer, including those of the mouth, pharynx, larynx, esophagus, stomach, and liver. Alcohol also interacts synergistically with tobacco to create cancer risks that are significantly greater than the sum of the effects produced by each acting alone. Limiting ones consumption of alcoholic beverages can therefore be an effective way of decreasing cancer risk.

Recommendations concerning alcohol consumption are complicated by the fact that unlike tobacco, which has no known health benefits, drinking moderate amounts of alcohol have been linked to about a 25% reduction in the risk of coronary heart disease.

The observation that the incidence of heart disease is relatively low in France despite high rates of saturated fat intake and smoking has led to the claim that red wine is particularly beneficial. However, epidemiological studies have failed to show a reliable difference in the heart benefits of drinking wine versus any other kind of alcohol.

Although alcohol’s beneficial effects on the heart have been fairly well established, these benefits are only seen at moderate levels of drinking—that is, no more than one to two drinks per day Alcohol consumption in excess of these levels has no discernable health benefits and creates a variety of health hazards, including an increased risk of cancer.

Anyone considering modest levels of alcohol con­sumption to exploit its beneficial effects on the heart might want to consider their own medical and family history to determine whether they have any predispositions to cardiovascular disease (where alcohol may be helpful) or cancer (where alcohol is more likely to be harmful).

3. Essay on Cancer Prevention: (Around 450 Words)

Protecting against the Ultraviolet Radiation in Sunlight Reduces the Risk of Skin Cancer :

Skin cancer is the most frequent type of cancer worldwide but is among the easiest to prevent because its main cause—the ultraviolet radiation in sunlight—is well known and easy to protect against. Nonetheless, many people tend to be nonchalant about the dangers of sun­light and often fail to take adequate precautions to protect themselves, presumably because skin cancer is rarely fatal.

Such casual attitudes ignore the potential dangers of melanoma, a type of tumor whose tendency to metasta­size makes it the most lethal form of skin cancer. Melanomas represent only 5% of all skin cancers, but the 5% figure corresponds to enough cancer cases to place melanoma among the ten most common types of cancer.

Surveys have revealed that only one-third of Americans routinely take the three precautions that are most effective in preventing skin cancer:

(1) Restricting exposure to the sun, especially during midday when its ultraviolet radiation is the strongest;

(2) Wearing protective clothing; and

(3) Using sufficient amounts of sunscreen lotion.

Modern sunscreen lotions typically contain a mixture of ingredients for blocking and absorbing both UVB and UVA radiation. The strength of any given sunscreen is expressed by its SPF (sun-protection factor), a number that reflects how much time it takes for skin treated with sunscreen to burn compared with unprotected skin.

In other words, an SPF of 15 means that skin covered with sunscreen lotion will take 15 times longer to burn than unprotected skin. If it would normally take your skin 20 minutes to burn under a given set of sunlight conditions, proper use of a sunscreen lotion with an SPF of 15 would allow an exposure of 20 × 15 = 300 minutes (5 hours) before burning.

However, people typi­cally apply sunscreen in amounts that achieve only about half of the protection suggested by the SPF value. Thus in actual practice, a sunscreen labeled with an SPF of 30 needs to be used to achieve an SPF of 15.

It has been estimated that worldwide death rates from melanoma could be reduced by at least 50% if people restrict their exposure to intense sunlight, wear protective clothing, and properly use sunscreens that achieve an SPF of at least 15. In Australia, which has the highest incidence and death rates for skin cancer in the world, significant public education efforts have been made to try to influence sun-related attitudes and behaviors.

Three years after the launching of one prevention program in the Australian state of Victoria, the rate of sunburn dropped by 35% and people reported an increase in the wearing of hats and the use of sunscreen. Such results indicate that exposure to melanoma risk factors can be reduced fairly rapidly in response to health promotion campaigns.

4. Essay on Cancer Prevention: (Around 550 Words)

Cancer Risks Created by Ionizing Radiation Tend to be Small for most Individuals :

Ionizing radiation is a high-energy type of radiation that removes electrons from molecules, thereby generating reactive ions that trigger DNA damage. Although large- dose exposures to ionizing radiation can cause many types of cancer, the doses encountered by the average person tend to be relatively small and account for less than 5% of all cancers.

Most of the ionizing radiation encountered on a regular basis—other than from the radioactive polonium in tobacco smoke—comes from natural background sources that cannot be readily avoided. The largest con­tributor to background radiation is radon, a radioactive gas emitted from underground rock formations in the earth’s crust.

Increased rates of lung cancer have been detected in underground mine workers exposed to high concentrations of radon for long periods of time, but comparable exposures are rarely experienced by the general public. Nevertheless, radon gas can seep into homes and accumulate in significant amounts if the venti­lation is inadequate, especially in regions of the country where large amounts of radon are emitted from the earth’s surface.

It is therefore advisable to test for radon levels in the home and, if they are exceptionally high, install an improved ventilation system in the basement to minimize the amount of radon that accumulates. Inexpensive radon testing kits suitable for this purpose are readily available at hardware stores or through public health agencies.

Natural background radiation accounts for about 80% of the ionizing radiation encountered by the average person. Of the remaining 20%, medical X-rays make the largest contribution. The health benefits of medical X-rays almost always outweigh the small risks involved, as long as X-rays are used only when a clear medical necessity exists.

A striking example of the dangers associated with unnec­essary medical X-rays occurred in the mid-1900s, when X-ray treatments were employed for clearing up facial acne in adolescent children. Individuals who received these treatments later developed thyroid cancer at signifi­cantly elevated rates.

Caution is also appropriate when using a high-dose X-ray procedure known as a computed tomography scan (CT scan) with young children. CT scans deliver up to 100 times more radiation than standard medical X-rays, and growing children are more sensitive than adults to the hazards of ionizing radiation.

In general, the average citizen tends to overestimate the risks posed by ionizing radiation. For comparison purposes, it is worth pointing out that among the Japanese residents of Hiroshima and Nagasaki who survived the immediate effects of the atomic explosions in 1945, only about 1% have died of radiation-induced cancers despite receiving radiation doses that were enormously greater than most people will encounter in their entire lifetimes.

Another interesting comparison involves perceptions regarding the dangers of the radiation associated with nuclear power. Living near a nuclear power plant normally exposes people to a radia­tion dose that is less than 1% of the background radiation we all receive from natural sources.

Yet when individuals are asked to rank their perceived risk of dying from various activities, nuclear power tends to be ranked ahead of much riskier activities, such as smoking cigarettes. In reality, the risk of dying from a radiation-induced cancer is quite small compared to most of the other risks associated with everyday life.

5. Essay on Cancer Prevention: (Around 450 Words)

Avoiding Exposure to Certain Infectious Agents can Reduce Risks for Several Types of Cancer :

Although cancer is not usually perceived by the general public as being an infectious disease, roughly 15% of all cancers worldwide are linked to viral, bacterial, or para­sitic infections. People can therefore lower their risk of developing cancer by avoiding behaviors that expose them to the relevant infectious agents.

Human papillomavirus (HPV) is responsible for the largest number of virally linked cancers, mainly cervical cancer and, to a lesser extent, cancer of the penis. HPV is spread predominantly through sexual activity, so the risk of becoming infected can be reduced by avoiding sexual contact with multiple partners.

Using a condom also decreases the risk of HPV-induced cancers, but condoms are not fully protective because they fail to prevent the spread of HPV caused by contact with infected areas not covered by the condom.

The hepatitis B and hepatitis C viruses are responsible for most cases of liver cancer, a common form of cancer in Southeast Asia, China, and Africa. The hepatitis B virus is transmitted by exchange of bodily fluids, such as blood or semen, and can be easily spread through sexual activity. The proper use of latex condoms may help reduce the transmis­sion of hepatitis B, although the efficacy of the protection is unknown.

The hepatitis C virus is difficult to transmit by mechanisms other than direct contact with contaminated blood, so the main route for acquiring hepatitis C is through the sharing of dirty needles by intravenous drug users. Hepatitis viruses can also be transmitted by blood transfusions involving contaminated blood, but the blood supply used for medical purposes is now routinely screened for both the hepatitis B and hepatitis C viruses.

The only bacterium to be clearly linked to a human cancer is H. pylori, the main cause of stomach cancer. Roughly half the world’s population has been infected with H. pylori, and stomach cancer is therefore one of the top cancer killers globally.

Unlike the situation in many coun­tries, the prevalence of stomach cancer in the United States has declined substantially over the past several decades. One factor contributing to this marked decline is the widespread use of antibiotics, which has diminished the rate of H. pylori infections and thereby reduced the chances that people will come in contact with infected individuals.

Public health conditions also play an important role because transmission of H. pylori from person to person is facilitated by poor sanitation and crowded living environ­ments, which are less prevalent in the United States than in most developing countries (Figure 4).

6. Essay on Cancer Prevention: (Around 750 Words)

Minimizing Exposure to Cancer-Causing Chemicals and Drugs can Reduce Cancer Risks :

More than two hundred chemical substances are known to cause—or are reasonably anticipated to cause—cancer in humans. These carcinogens are identified through the combined use of epidemiological evidence, animal testing, and the Ames test.

In practice, many of the chemicals that pose a signifi­cant cancer risk for humans were not identified until large numbers of cancers had arisen in workers exposed to these substances on a regular basis, especially in the rubber, chemical, plastic, mining, fuel, and dye industries. Although some of the responsible chemicals have now been banned from the workplace, others remain in use.

Workers must therefore take appropriate precautions, such as wearing masks and protective clothing, working in properly ventilated environments, and in some cases breathing through a respirator. As a result of the protec­tive measures that have been implemented, many of the occupational cancers that were once prevalent in the United States have declined in frequency, and workplace exposure to carcinogenic chemicals now accounts for less than 5% of all fatal cancers.

Chemical carcinogens are usually encountered in high concentration only in industrial workplaces or in tobacco smoke, but small amounts escape into the envi­ronment and contaminate the air we breathe, the water we drink, and the food we eat. It has therefore become fashionable to blame chemical pollution of the environ­ment for creating a cancer epidemic.

In fact, the data do not generally support this conclusion. Those chemical carcinogens that do pollute the environment tend to be present in concentrations that are thousands of times lower than typical workplace exposures, and most evi­dence suggests that the cancer threat they pose for the average person is quite small.

Of course, not everyone is an “average person” . For example, people who live near a site where toxic chemicals have been stored or released may be exposed to carcinogen concentrations that are thousands of times higher than those encountered by the general public.

Similarly, people who live in older buildings constructed with asbestos- containing materials may have higher-than-normal exposures to asbestos, especially if the construction mate­rials are deteriorating. Each person therefore needs to assess his or her own living situation to determine whether it involves any unusual contact with carcinogenic chemicals.

People also encounter high concentrations of specific chemicals when they take prescription drugs to treat chronic health problems. If a single drug is used for a protracted period of time, exposure to the substance in question will be high and it is important to know whether any cancer risks are involved.

There are number of pre­scription drugs that are already known to cause cancer. Because of the cancer hazard, most of these drugs are only prescribed for serious medical conditions in which the potential benefits of the drug in question far outweigh the risk that cancer might arise.

One problem in assessing the cancer hazards associ­ated with prescription drugs is that many years of human use may be required before the risks become apparent. For example, diethylstilbestrol (DES) is a synthetic estrogen that was prescribed to pregnant women for 30 years before its carcinogenic properties were discovered.

A more recent illustration is provided by hormone replacement therapy (HRT), a treatment sometimes prescribed for postmenopausal women because their lowered estrogen production can lead to several health problems, including increased risks for heart disease and osteoporosis (bone loss).

In the 1950s and 1960s, doctors routinely prescribed estrogen pills to postmenopausal women to prevent these problems. Then it was reported in the mid-1970s that estrogen administration creates an increased risk for uterine (endometrial) cancer, and its use began to decline.

When subsequent studies showed that the uterine cancer risk can be reduced or eliminated by combining estrogen with a progestin (a substance exhibiting progesterone-like activity), estrogen-progestin became the predominant form of HRT.

Although this newer type of HRT was initially thought to be safe, a study of 16,000 postmenopausal women sponsored by the Women’s Health Initiative was prematurely halted in 2002 when results began to suggest that the harmful effects associated with estrogen- progestin treatment outweigh the potential benefits.

One of the main problems to be reported was an increased incidence of breast cancer, but elevated rates for strokes, heart attacks, and blood clots were noticed as well. While the study also revealed that estrogen-progestin treatment lowers the risk of osteoporosis and colon cancer, these benefits were not considered to be sufficient to outweigh the other risks (Figure 5).

In 2003, a Swedish trial of HRT in postmenopausal women with a previous history of breast cancer was also halted, in this case because of an unacceptably high recurrence rate for breast cancer.

7. Essay on Cancer Prevention: (Around 650 Words)

Reduced Consumption of Saturated Fat, Red Meat, Total Calories, and Dietary Carcinogens may Decrease Cancer Risk :

Of the thousands of chemicals we routinely encounter on a daily basis, most that enter our bodies are deliberately ingested because they are natural components of food. People who differ in the foods they eat also tend to differ in the cancers they develop, suggesting that diet has an important influence on cancer risks.

Unfortunately, the effects of individual foods are difficult to pinpoint because the eating habits of different people vary in numerous ways, making it hard to assess the impact of each ingredient.

The situation is further complicated by the fact that in any given diet, the carcinogenic effects of a substance found in one type of food may be blocked by the protective action of another substance present in the same diet.

In other words, cancer risk is related both to foods that increase cancer risk (whose intake should be reduced) and to foods that decrease cancer risk (whose intake should be increased).

It has been widely recommended that one component of the diet whose consumption should be reduced is animal fat. Unlike the fats found in fruits and vegetables, which are largely unsaturated, animal fats are rich in saturated fat. (The term saturated refers to a fat molecule in which all carbon atoms are bound to the maximum number of hydrogen atoms.)

Diets rich in saturated fat in general, and red meat in particular, have been linked in numerous epi­demiological studies to an elevated risk for several types of cancer, including colon, prostate, and breast cancers.

The main problem with this evidence is that most of the early epidemiological studies involved a retrospective approach in which people who had already developed cancer were asked to recall their dietary habits from many years earlier.

Because retrospective studies are susceptible to numerous sources of bias, several recent studies have used the more powerful prospective approach in which large groups of individuals without cancer are monitored into the future to see who develops the disease. Participants are repeatedly asked about their eating habits along the way, which provides more reliable information than can be obtained by asking people for their recollections many years later.

Large studies of this type have continued to support the conclusion that eating red meat is a risk factor for colon cancer, although the relationship between saturated fat intake and cancer risk is less certain. Part of the reason for this uncertainty may be that even large prospective studies are hampered by imprecise methods for assessing what people really eat.

The apparent linkage seen in some studies between saturated fat intake and cancer risk may arise in part because fats have higher calorie content than other nutrients. Two reasons exist for believing that extra calories are a cancer risk.

First, animal studies have shown that reducing the number of calories in the diet leads to a decrease in cancer rates, both for spontaneous tumors and for tumors induced by carcinogenic chemicals or radiation (Figure 6).

Second, people who eat high-calorie diets are in danger of becoming overweight, especially if they do not exercise regularly.

In addition to reducing red meat, saturated fat, and calorie intake, several other approaches exist for decreasing cancer hazards in the diet. One is to reduce the use of high-temperature cooking techniques, such as open flame grilling or deep frying, which generate carcinogenic polycyclic aromatic hydrocarbons and aromatic amines that were not initially present in the foods being cooked. Food preservation techniques are another potential source of dietary carcinogens that can be avoided.

For example, decreased consumption of foods that are smoked, cured, pickled, or heavily salted has been linked to a lower risk for stomach cancer. Taking simple measures to reduce pesticide contamination, such as washing or peeling fruits and veg­etables, is also a reasonable precaution, although the potential hazards of pesticide contamination are probably overemphasized.

8. Essay on Cancer Prevention: (Around 1000 Words)

Reducing Exposure to Carcinogens Involves a Combination of Personal and Governmental Actions :

There are two basic ways in which exposure to carcino­gens can be decreased. One is for individuals to take personal actions like those we have been discussing—that is, reducing exposure to tobacco smoke, alcohol, sunlight, ionizing radiation, cancer-causing infectious agents, and chemical carcinogens encountered in the workplace, drugs, and the diet. (Of course, people need to be edu­cated about these dangers before they can be expected to take action.) The second approach is for the government to create laws and regulations that reduce or eliminate the carcinogenic hazards to which people are exposed.

In practice, the two approaches tend to complement each other. A good illustration of this principle is provided by the history of cigarette smoking in the United States. Smoking rates increased dramatically in the twentieth century until 1964, the year in which the first Surgeon General’s Report on Smoking and Health was published (see Figure 1).

This report concluded that cigarette smoking causes lung cancer and stated, “Cigarette smoking is a health hazard of sufficient importance in the United States to warrant appropriate remedial action” . As a consequence, Congress passed the Federal Cigarette Labeling and Advertising Act of 1965 and the Public Health Cigarette Smoking Act of 1969.

These laws required health warnings on cigarette packages, restricted cigarette advertising, and called for periodic government reports on the health consequences of smoking. Over the ensuing decades a growing body of federal and local regulations imposed further controls, including restrictions on smoking in public places, airplanes, office buildings, restaurants, and the workplace.

Despite the severe health hazards involved, there has been no attempt to ban cigarettes outright, an approach that would clearly be impractical. Government and public health organizations have instead worked to educate people about the dangers of smoking and to promote a nonsmoking cul­tural environment that encourages individuals to make their own personal decision not to smoke.

This strategy has been fairly successful- Smoking rates have gradually declined over the past 40 years and people are giving up smoking in increasing numbers. In fact, nearly half of all living Amer­ican adults who ever smoked have now quit, and smoking rates among men have fallen by roughly 50% since 1964.

OSHA and the FDA are Governmental Agencies that Regulate Carcinogens in the Workplace and Food Supply :

Government involvement in protecting the public from carcinogenic hazards is not restricted to tobacco products. Another area of interest is the industrial workplace, where employees may be exposed to high doses of chemical carcinogens for prolonged periods of time.

In the first half of the twentieth century, many cancers were caused by such occupational exposures before the risks were fully appreciated. Finally, in 1970 an act of Congress created the Occupational Safety and Health Administration (OSHA) to formulate and enforce regulations that protect the safety and health of workers.

OSHA regulations have eliminated some of the most dangerous carcinogens from the workplace and have created requirements that limit worker exposure to others. As a consequence, occupational cancers that were once prevalent in the United States are declining in frequency and now account for less than 5% of all cancer deaths each year.

Regulation of carcinogens in the food supply has had a more complicated history. In the United States, food additives and contaminants that might cause cancer are regulated by the Food and Drug Administration (FDA), a federal agency whose jurisdiction includes most foods other than meat.

A law passed in 1938 empowered the FDA to prohibit the marketing of any food containing a substance that may render it injurious to health. In 1958, Congress passed the Delaney Amendment, which specifically directed the FDA to ban any food additive or contaminant if it was found to cause cancer in animals at any dose.

The Delaney Amendment, which expired in 1996, was referred to as a zero-risk standard because it allowed for no acceptance of even the tiniest amount of an additive or contaminant in food once it has been shown to exhibit any carcinogenic properties in animals.

Using the authority provided by the preceding laws, the FDA has banned a number of food additives and contaminants suspected of being human carcinogens. Among the prohibited substances are several food- coloring agents (e.g., Red No. 2 and Red No. 4), artificial sweeteners (e.g., cyclamate), and packaging materials that contaminate food (e.g., acrylonitrile used in making plastic beverage bottles). When the FDA attempted to ban the artificial sweetener saccharin, however, the difficulties inherent to its approach for assessing carcinogenic hazards became evident.

Saccharin is an artificial sweetener with a long history of use in foods and beverages. After several studies showed that saccharin causes bladder cancer in laboratory animals, the FDA proposed in 1977 to prohibit its use based on the requirements of the Delaney Amendment.

At that time, saccharin was widely used in diet foods— millions of pounds were consumed annually in soft drinks alone—and a public outcry ensued. In response, Congress passed a law overriding the FDA ban and saccharin remained legal. However, the law did require a warning label on saccharin-containing foods and beverages indicating that saccharin causes cancer in animals.

In 1981, the government used this animal evidence as justification for placing saccharin on its list of substances that are “reasonably anticipated” to be human carcinogens. Twenty years later, the government reversed its position and saccharin was removed from the list. The reason for the reversal was a series of studies showing that the original animal data, derived mainly from rats, were not likely to be relevant to humans.

The newer experiments revealed that saccharin causes bladder cancer in rats by binding to proteins in the urine, thereby triggering the formation of calcium phosphate-containing crystals that irritate the bladder wall and lead to cancer. Formation of these crystals requires the presence of high concentrations of calcium phosphate and protein in the urine, conditions unique to the rat bladder that do not exist in humans.

9. Essay on Cancer Prevention: (Around 800 Words)

Regulatory Standards for Environmental Pesticides and Pollutants are Established Using Quantitative Assessments of Risks and Benefits :

The history of government efforts to regulate saccharin shows how difficult it can be to make decisions about food additives or contaminants that act as weak carcinogens in animals but may or may not cause cancer in humans. In the case of pesticides that contaminate the food supply, the situation is further complicated by the fact that different standards have been applied to raw and processed foods.

For many years pesticide contaminants detected in processed foods were considered to be additives covered by the Delaney Amendment, which imposed a standard of zero tolerance for any substance that causes cancer in animals. If the same pesticide happened to be detected in raw foods, the risk was analyzed quantitatively based on all available animal and human evidence so that an acceptable tolerance level could be established based on typical dietary intake.

Because of the confusion created by this inconsistent approach to pesticide regulation, Congress passed the Food Quality Protection Act of 1996 to eliminate the distinction between standards for raw and processed foods.

All pesticide residues are now regulated under the standard of “reasonable certainty of no harm,” which means that acceptable tolerance levels are established based on an assessment of what is thought to be safe.

Unlike the zero-tolerance standard of the Delaney Amendment, which does not discriminate between potent and weak carcinogens, the newer type of analysis establishes different tolerance levels for carcinogens of differing potency. Moreover, benefits as well as risks associated with the use of each pesticide are considered when establishing such standards.

The Environmental Protection Agency (EPA) uses a similar approach when creating regulatory standards for carcinogens that contaminate the environment. An instructive example is provided by the environmental carcinogen arsenic, which is present in trace amounts in the drinking water of many wells and municipal water systems.

Before 2001, the EPA regulatory standard for arsenic in drinking water had been set at 50 parts per billion (ppb). When epidemiological studies revealed that people who regularly drink water containing that much arsenic add about 1% to their lifetime risk of dying of cancer, the EPA proposed to lower the arsenic standard from 50 to 10 ppb.

In an ideal world, any proposal to reduce the threat from an environmental carcinogen would be immediately accepted, but in the real world of limited financial resources, the cost of each regulatory decision needs to be balanced against the benefits to be gained. It was estimated that the public and private spending required to lower the arsenic levels in drinking water from 50 to 10 ppb would range between $600,000 and $6,000,000 per avoided cancer death.

Although the EPA eventually decided that reducing arsenic levels was worth the expenditure, there is a point at which the cost of reducing the concentration of a given environmental carcinogen to a lower level becomes so great as to make the proposed effort impractical.

Since it is impossible to create a completely risk-free world in which all carcinogens have been removed, society needs to find ways of establishing priorities as to which carcinogenic hazards require the most attention. When establishing such priorities, two variables are particularly relevant. First, how potent is each carcinogen? Second, how much are we exposed to? These two variables have been combined into a single measure called the HERP value, where HERP stands for Human Exposure and Rodent Potency.

The HERP value for any given agent is calculated by determining the typical human lifetime dose of the substance in question and dividing it by the dose administered to mice or rats that causes half the animals to develop tumors within their lifetime. The HERP value is thus a measure of potential hazard that takes into account both human exposure and carcinogenic potency in animals.

In other words, powerful carcinogens with large human exposures exhibit the highest HERP values; weak carcinogens with small human exposures have the lowest HERP values, and potent carcinogens with small human exposures, or weak carcinogens with high human exposures, exhibit intermediate HERP values.

HERP calculations are not precise indicators of human hazard because of the uncertainties involved in extrapolating data on carcinogenic potency from animals to humans. Nonetheless, comparing the HERP values of various carcinogens with one another can provide insights as to which ones are likely to be most hazardous (Table 1). Such analyses have revealed that workplace exposures to chemical carcinogens tend to have high HERP values and therefore deserve considerable atten­tion.

In contrast, the pesticides and pollutants that contaminate our environment, water, and food supply generally exhibit HERP values that are quite low when compared with the background of naturally occurring carcinogens encountered in a typical diet.

10. Essay on Cancer Prevention: (Around 1500 Words)

Proposed Role of Fruits and Vegetables in Protecting against Cancer is Based Largely on Retrospective Studies :

During the past twenty years, the possible effectiveness of fruits and vegetables in reducing cancer risk has been investigated in more than 200 epidemiological studies. These investigations have consistently (but not univer­sally) supported the conclusion that people who eat more fruits and vegetables have lower cancer rates than people who eat fewer fruits and vegetables.

The association is strongest for cancers involving gastrointestinal and respiratory organs, such as stomach, colon, and lung cancers, and is weak for hormone-related cancers, such as breast and prostate cancers.

Unfortunately, interpreting the significance of the epidemiological evidence is complicated by two factors:

(1) The observed reductions in cancer rates are generally small, and

(2) Most of the early studies involved a retrospective approach in which people with cancer were asked to recall their previous dietary habits.

Retrospective studies are susceptible to several sources of bias and are generally less reliable than prospective studies that monitor healthy people into the future to see who develops cancer. When large prospective studies have been carried out, they generally detect little or no connection between overall fruit and vegetable consumption and cancer incidence.

This inconsistency in the epidemiological evidence has created some uncertainty regarding the precise role played by fruits and vegetables in protecting against cancer. Part of the problem may be that “fruits and vegeta­bles” is an imprecise label that includes dozens of different food items, only some of which may be useful in reducing cancer risk.

Because of the difficulty in comparing conclu­sions from different studies in which the exact food items are not clearly identified, we need to focus on individual fruits or vegetables—and the molecules they contain—to determine what roles, if any, these foods play in protecting against cancer.

Vitamins, Minerals, and Dietary Fiber are being Investigated as Possible Sources of Protection against Cancer :

A variety of natural substances present in fruits and vegetables have been investigated as possible sources of anticancer activity. Early research focused mainly on vitamins and minerals, which are known to be essential components of a healthy diet.

Vitamins A, B6, folic acid, B12, C, D, and E and the minerals calcium, iron, zinc, and selenium are among the vitamins and minerals that have been suggested to play a protective role against cancer.

Dietary intake of each of these substances has been linked to decreased cancer rates in some reports; other studies, however, have failed to confirm the results, and there is currently insufficient high-quality data to justify strong conclusions.

Further progress requires a better understanding of how vitamins and minerals exert their postulated anti­cancer effects. One property shared by several of these substances is their ability to act as antioxidants—that is, inhibitors of oxidation reactions. Carcinogenic chemicals and radiation sometimes cause DNA damage through oxi­dation reactions involving free radicals, which are atoms or molecules possessing an unpaired electron.

A free radical is a highly unstable substance that quickly attacks another nearby molecule, taking an electron that it needs to gain stability (Figure 7). Upon losing an electron, the second molecule also becomes a free radical and removes an electron from a third molecule, starting a chain reac­tion of oxidation reactions (oxidation refers to the process of losing an electron).

An uncontrolled cascade of free radical reactions can create considerable damage within a cell, including DNA mutations. Antioxidant vitamins halt this scenario by acting as free radical scavengers that donate their own electrons to free radicals without becoming unstable in the process.

For example, ascorbic acid (vitamin C) readily donates electrons to free radicals, undergoing oxidation to dehydroascorbic acid in the process. Dehydroascorbic acid is then converted back to ascorbic acid through a simple metabolic reaction and the process is repeated again.

The ability of antioxidant vitamins to function as free radical scavengers has led to the proposal that they might be able to inhibit carcinogenesis by preventing oxidative DNA damage. The principal antioxidant vitamins found in fruits and vegetables are vitamins A, C, and E.

Many retrospective studies have indicated that people who report high intake of these vitamins—either from food or through vitamin supplements—exhibit decreased cancer rates. The effects are generally small, however, and could easily be caused by other unmeasured differences in lifestyle or environment. The only way to provide convincing proof would be a randomized trial in which participants are randomly assigned to receive either a vitamin supplement or a placebo.

During the mid-1980s, a randomized trial of vitamins A and E was initiated in Finland to see whether these vita­mins can reduce lung cancer rates, as was suggested by earlier retrospective evidence. The Finnish trial involved more than 29,000 male smokers who were randomly assigned to receive vitamin A (in the form of beta-carotene), vitamin E, both, or neither (placebo).

Over a period of seven years, the trial failed to detect any protective effect of either of the two vitamins on lung cancer rates. In fact, a statistically significant increase in lung cancer cases was actually observed in the men who received vitamin A supplements (Figure 8).

A second independent study carried out in the United States confirmed the ability of vitamin A to increase lung cancer rates. Such results cast serious doubt on the usefulness of vitamin A for cancer protection and reveal the possible risks associated with using vitamins in high doses (the amounts of vitamin A employed in these studies were five to ten times higher than the normally recommended dietary intake).

The preceding results do not rule out the possibility that certain vitamins might exhibit some useful anticancer properties when consumed directly from a well-balanced diet or obtained from pills designed to deliver normally recommended vitamin doses rather than high doses. One vitamin thought to protect against cancer in normal doses is folic acid.

The typical dietary intake of folic acid in the United States is less than optimal, and low intake of folic acid can lead to DNA damage (folic acid normally provides the methyl group needed for synthesizing the base thymine in DNA). The possibility that low intake might create an increased cancer risk is supported by reports of increased colon cancer rates in people whose diets are deficient in folic acid.

In one long-term prospective study, a 75% reduction in colon cancer rates was seen in individuals who take multivitamin pills containing folic acid, although the effect did not become evident until the vitamins were used for 15 years (Figure 9).

An obvious problem in such studies is that multivitamin pills contain a variety of dif­ferent vitamins and minerals, and it is possible that ingredients other than (or in addition to) folic acid were responsible for the reduction in cancer rates. Vitamin D, for example, is thought to exert some protective effects against colon cancer and might have contributed to the observed reduction in cancer rates.

The ideal test would involve a randomized trial of folic acid or vitamin D versus placebo pills, but it is generally impractical to run trials for the long duration required in this particular case (15 years).

Vitamins are not the only constituents of fruits and vegetables for which it has been difficult to obtain reliable evidence. A similar situation exists with dietary fiber, the indigestible portion of plant foods that is composed mainly of complex polysaccharides.

Early retrospective studies suggested that colon cancer rates are decreased in people who consume large amounts of dietary fiber, but most of these studies included little information regarding other components of the diet and did not permit the effects of fiber to be clearly distinguished from the effects of other components of plant foods.

The retrospective nature of the studies also raised the possibility of numerous sources of bias, including the problem of asking individuals with cancer to recall their dietary habits from many years earlier. Large prospective studies, which tend to be more reliable, have generally found little relationship between dietary fiber intake and colon cancer protection.

It has been suggested, however, that the populations being studied do not vary sufficiently in fiber intake to detect an effect. One large prospective study of European populations, which tend to exhibit substantial variability in fiber intake, has reported that doubling the average fiber intake is associated with a 40% reduction in colorectal cancer incidence.

11. Essay on Cancer Prevention: (Around 1200 Words)

Fruits and Vegetables Contain Dozens of Phytochemicals that Exhibit Possible Cancer-Fighting Properties :

Although early investigations focused largely on vitamins and minerals, fruits and vegetables contain many other substances that might play roles in blocking or slowing cancer development. The collective term phytochemicals is commonly used when referring to this large group of plant-derived molecules.

Technically speaking, any chemical produced by a plant is a “phytochemical”; the term is usually restricted, however, to plant chemicals that are thought to have health-related effects but are not essential nutrients like proteins, carbohydrates, fats, minerals, and vitamins.

Phytochemicals are a structurally diverse group of molecules that exhibit a wide range of properties with potential relevance for fighting cancer. Among the most relevant properties are the abilities to inhibit carcinogen activation, stimulate carcinogen detoxification, inhibit carcinogen binding to DNA, inhibit free radical and other DNA-damaging oxidative pathways, inhibit cell prolifera­tion, inhibit oncogene expression, induce apoptosis, induce differentiation, inhibit angiogenesis, and inhibit invasion and metastasis. Laboratory studies have identified dozens of phytochemicals that might help protect against cancer through one or more of these mechanisms.

A few representative examples are illustrated in Figure 10 and briefly described below:

1. Lycopene:

Lycopene is a natural red pigment that gives tomatoes and other fruits and vegetables their reddish colors. The chemical structure of lycopene is related to that of beta-carotene (a vitamin A precursor), and, like beta- carotene, lycopene is a potent antioxidant. Epidemiological studies have linked dietary intake of lycopene, derived mainly from tomatoes and tomato-based sauces, to a reduced incidence of several cancers, especially those of the prostate, lung, and stomach.

In some cases, lycopene levels have been directly measured in blood samples to verify dietary intake. Such measurements have shown that individ­uals with higher concentrations of lycopene in their blood exhibit lower rates of cancer than people with lower concen­trations.

Lycopene’s antioxidant properties are thought to be responsible for the lowering of cancer risk, but lycopene also exerts other effects on metabolism, gene activity, and cell signaling that might be involved.

2. Isothiocyanates:

Isothiocyanates are a diverse group of compounds, characterized by the presence of a—N=C=S group, that occur in especially high concentration in the vegetable family that includes broccoli, brussels sprouts, cabbage, cauliflower, and watercress. Broccoli, for example, contains large amounts of an isothiocyanate called sulforaphane, and watercress contains large amounts of phenethyl isothiocyanate.

Isothiocyanates are potent inhibitors of tumor formation when tested in animals exposed to chem­ical carcinogens, and complete inhibition of cancer formation by relatively low doses of isothiocyanates is often observed.

The ability of isothiocyanates to block cancer development stems mainly from two properties: the ability to inhibit pathways for carcinogen activation and the ability to stimulate pathways for carcinogen detoxification. Many isothiocyanates exhibit one property or the other, and some exhibit both.

3. Epigallocatechin gallate:

Numerous animal and labora­tory experiments, along with some human epidemiological studies, have indicated a possible benefit of green tea in protecting against certain cancers, especially those of the esophagus, stomach, colon, and bladder. The substance epigallocatechin gallate (EGCG), which is present in high concentration in green tea, exhibits a number of properties that may help explain how green tea could protect against cancer.

Among these properties are the abilities of EGCG to act as an antioxidant, inhibit carcinogen activation, stimulate carcinogen detoxification, inhibit cell proliferation, induce cell cycle arrest, induce apoptosis, and inhibit angiogenesis. It remains to be determined, however, if any of these activities are exerted to a significant extent by the small amounts of EGCG a person typically ingests when drinking green tea.

4. Isoflavones:

Breast and prostate cancer rates are rela­tively low in Japan and China, where soybean-derived foods represent a significant portion of the diet. A group of soybean compounds known as isoflavones have been proposed to play a role in these reduced cancer rates. One isoflavone, called genistein, exhibits weak estrogen-like effects on the body and is therefore referred to as a phytoestrogen ( “plant estrogen” ).

The growth of breast cancer cells in culture is inhibited by high concentrations of genistein, suggesting that this isoflavone can act as an antiestrogen. However, at lower concentrations that may be closer to levels seen in humans who eat soy products, genistein has been reported to stimulate breast cell proliferation. Given this potential to either inhibit or stimulate breast cell proliferation, a precautionary approach to consuming soy to prevent breast cancer is advisable until the role of soy isoflavones is better understood.

5. Resveratrol:

Resveratrol, an antioxidant produced by a variety of plants, is present in especially high concentration in the skin of red grapes and in red wines made from these grapes. It has been proposed that resveratrol is responsible for the reported linkage between red wine consumption and lower death rates from cardiovascular disease and certain cancers.

In addition to acting as an antioxidant, resveratrol exhibits a number of other properties that might be relevant to cancer prevention. For example, resveratrol can promote carcinogen detoxification, inhibit DNA mutation, inhibit cell proliferation, and induce apoptosis. Resveratrol also inhibits the synthesis and metabolic activity of cyclooxygenases, which are enzymes whose role in promoting inflammation and stimulating tumor cell growth will be described shortly.

6. Sulfides:

For more than 3000 years, folklore has advocated garlic as a remedy for a variety of health problems. Recent epidemiological studies have provided some support for these beliefs by linking high levels of garlic consumption with reduced cancer rates, especially for cancers of the stomach, colon, and prostate. Garlic contains a variety of organic sulfides (compounds containing sulfur joined to carbon by single bonds) that might be relevant to the postulated benefits of garlic.

For example, a compound called diallyl sulfide, which is present in high concentration in garlic, has been shown to inhibit the development of colon, esophageal, and lung cancers in animals that have been exposed to chemical carcinogens. Organic sulfides exhibit a number of properties of potential relevance to cancer protection, including the ability to inhibit carcinogen activation, stimulate DNA repair, inhibit cell proliferation, and induce apoptosis.

The preceding list includes only a few of the numerous phytochemicals that are currently being investigated. The reported existence of cancer-preventing properties in these molecules is certainly encouraging, but a note of caution is appropriate because most investigations are still in their early stages.

For comparison purposes, it is worth pointing out that the initial body of evidence regarding the postulated role of vitamin A in preventing cancer was also very encouraging, but randomized human trials eventually revealed that the early claims were unjustified.

Since the cancer-fighting properties of phytochemicals have not been evaluated in randomized human trials, it would be premature to draw any definitive conclusions regarding their usefulness in preventing cancer.

12. Essay on Cancer Prevention: (Around 750 Words)

Aspirin and Other Anti-Inflammatory Drugs may Help Prevent Certain Types of Cancer :

Thus far, we have been focused on inhibiting cancer development through the use of substances present in food, either by eating specific foods or by ingesting some of the chemicals they contain, such as vitamins, minerals, and phytochemicals.

This practice of using specific chemical substances for protecting against cancer is called chemoprevention. Besides natural substances found in foods, a variety of synthetic drugs are also being explored for possible use in cancer chemoprevention efforts.

One drug known to be helpful in protecting against cancer is aspirin. The synthesis of aspirin was first reported in the late 1890s by Felix Hoffmann, a German chemist who was searching for a way to relieve his father’s arthritis pain. Motivated by folklore concerning the pain- relieving and anti-inflammatory properties of willow bark, Hoffman synthesized aspirin from an ingredient in willow bark called salicylic acid.

The ability of aspirin (acetylsalicylic acid) to reduce pain, fever, and inflamma­tion with minimal short-term toxicity has made it the world’s most widely used medication. Aspirin works by inhibiting the enzyme cyclooxygenase (COX), which catalyzes the production of chemical messengers called prostaglandins.

Some prostaglandins act on blood vessels, nerves, and cells of the immune system to trigger tissue inflammation, which is characterized by swelling, redness, pain, and heat. By inhibiting cyclooxygenase, aspirin reduces prostaglandin production and thereby diminishes these symptoms.

During the 1990s, a series of retrospective and prospective epidemiological studies revealed that people who use aspirin on a regular basis exhibit up to a 50% reduction in colon cancer rates. Lower rates for several other types of cancer were reported as well, including cancers of the prostate, lung, mouth, throat, and esophagus.

Such results suggest that aspirin might be a simple and effective tool for cancer chemoprevention. Unfortunately, chronic use of aspirin has drawbacks because the drug also causes stomach irritation, bleeding, and ulcers. The reason for these side effects is that cyclooxygenase, the enzyme inhibited by aspirin, exists in multiple forms with differing functions.

One form, called COX-1, is expressed in many cell types and plays a variety of normal roles, such as protecting the lining of the stomach against acid irritation. Inhibition of COX-1 by aspirin interferes with this protective function, thereby triggering the adverse effects of aspirin on the stomach.

A second form of cyclooxygenase, called COX-2, is also inhibited by aspirin. Normal tissues contain relatively little COX-2 but production of the enzyme is enhanced at sites of tissue damage, where it synthesizes prostaglandins that trigger tissue inflammation. COX-2 is also produced by colon cancers and other epithelial malignancies, where it may contribute to tumor development by synthesizing a prostaglandin known as prostaglandin E2 (PGE2).

PGE2 exhibits several properties that could help cancer cells proliferate, survive, and evade the immune system. First, PGE2 inhibits the activity of cytotoxic T lymphocytes, which might otherwise attack tumor cells. PGE2 also stimulates angiogenesis, which is required for tumor growth beyond a tiny size, and it inhibits apoptosis in cancer cells. Each of these properties could play a role in cancer development and progression.

The discovery that COX-2 produces prostaglandins that trigger tissue inflammation and facilitate cancer development suggests that aspirin’s ability to decrease cancer risk stems from its inhibitory effects on COX-2. Aspirin’s adverse effects, such as stomach bleeding and ulcers, are linked to its inhibition of COX-1.

To obtain the beneficial effects of aspirin without the adverse side effects, several new anti-inflammatory drugs were intro­duced in the late 1990s that selectively inhibit COX-2 rather than inhibiting both COX-1 and COX-2 like aspirin does.

These selective COX-2 inhibitors, sold under the trade names Vioxx, Celebrex, and Bextra, were initially introduced to provide relief from chronic arthritis pain without causing the stomach problems seen with aspirin.

Preliminary evidence suggested that COX-2 inhibitors might also be useful for reducing colon cancer risk, and a large clinical trial was initiated in early 2000. Unfortunately, the trial was halted in late 2004 when it was discovered that COX-2 inhibitors double the risk of heart attack and stroke, and the future of these drugs is now uncertain.

Several other anti-inflammatory drugs in addition to aspirin—for example, acetaminophen (Tylenol) and ibuprofen—have also been reported to exhibit some protective effects against cancer, although the data are not nearly as extensive as for aspirin. The possible usefulness of these and other anti-inflammatory drugs for reducing cancer risk is likely to be an area of active future investigation.

13. Essay on Cancer Prevention: (Around 900 Words)

Hormone-Blocking Drugs are Potentially Useful for Preventing Hormone-Dependent Cancers :

Cancers arising in hormone-dependent tissues, such as the breast and prostate, are sometimes treated with drugs that interfere with the actions of the required hormones. For example, tamoxifen blocks the estrogen receptors of breast cells and inhibits the ability of estrogen to drive the prolif­eration of these cells, thereby making the drug useful for treating estrogen-dependent breast cancers.

Tamoxifen may also be helpful for preventing breast cancer in women at high risk for the disease. The rationale for this approach is related to events that normally control the proliferation of breast cells. During each menstrual cycle, estrogen triggers the proliferation of epithelial cells that line the milk glands in the breast.

If pregnancy does not occur, estrogen levels decline at the end of the men­strual cycle and those breast cells that have proliferated in that month deteriorate and die. For the average woman, the result is hundreds of cycles of cell division and death repeated over a span of roughly 40 years, from puberty to menopause.

These repeated cycles of estrogen-induced cell division increase the risk of developing cancer in two ways:

(1) Estrogen stimulates the division of any cells that may have already acquired DNA mutations, thereby increasing the number of mutant cells that might progress to malignancy; and

(2) Repeated cycles of estrogen-induced proliferation increase the chances of new mutations arising as a result of errors in DNA replication.

Because estrogen-driven proliferation of breast cells increases the risk of cancer, using tamoxifen to block estrogen action would be expected to lower the cancer risk. To test this hypothesis, the National Cancer Insti­tute sponsored a study during the 1990s that involved more than 13,000 healthy women considered to be at high risk for breast cancer based on either their family or medical history.

Half the women were given tamoxifen and the other half were given a placebo. Over a five-year period, the women receiving tamoxifen experienced a roughly 50% reduction in new cases of breast cancer (Figure 11).

If a reduction in breast cancer risk were the only effect of tamoxifen, the drug would be widely recommended for breast cancer prevention. Unfortunately, tamoxifen has a side effect that limits its usefulness. This side effect arises because tamoxifen does not block estrogen receptors in every tissue as it does in the breast.

In the uterus, tamoxifen mimics the action of estrogen when it binds to estrogen receptors; thereby stimulating cell proliferation and increasing the risk of uterine endometrial cancer (see Figure 11, right). Tamoxifen is therefore unsuitable as a cancer prevention drug in women with no obvious sus­ceptibility to breast cancer because of the elevated risk of developing uterine cancer.

Drugs like tamoxifen, which block estrogen action in some tissues but act like an estrogen in others, are called selective estrogen receptor modulators (SERMs) because they selectively stimulate or inhibit the estrogen receptors of different target tissues. Scientists have been working to develop other SERMs that might exhibit the beneficial properties of tamoxifen on the breast without its harmful effects on the uterus.

One example is raloxifene, a drug that is useful for preventing osteoporosis (bone loss) in postmenopausal women. Raloxifene functions like estrogen in bone, acting to maintain bone strength and increase bone density.

In contrast, raloxifene blocks estrogen action in the breast and uterus and has been shown to reduce the incidence of breast and uterine cancers in animal studies. The National Cancer Institute is therefore sponsoring a human trial called the Study of Tamoxifen and Raloxifene (STAR) to directly compare the effects of the two drugs in preventing cancer.

Prostate cancer is another type of cancer arising in a hormone-dependent tissue that might be preventable using drugs that block hormone action. Since the proliferation of prostate cells depends on steroid hormones called androgens (testosterone is one example), prevention efforts have focused on drugs that inhibit androgen activity.

One such drug, finasteride, is an enzyme inhibitor that blocks the production of dihydrotestosterone, the active form of testosterone in the prostate. In a randomized trial involving more than 18,000 men, daily use of finasteride was found to reduce the incidence of new cases of prostate cancer by 25% compared with the placebo group.

While these results suggest that hormonal prevention of prostate cancer might be an attainable goal, there are significant concerns about the use of finasteride for this purpose. The most serious problem is the discovery that men receiving finasteride in the randomized trial developed a higher proportion of high-grade cancers (37% of their tumors were high grade) than did the men who received the placebo (22% of their tumors were high grade).

So even though men receiving finasteride developed fewer cancers, the tumors that did develop were more aggressive on average than those observed in the control group. One possible explanation for this unex­pected result is that the androgen-deficient environment created by finasteride treatment may favor the develop­ment of tumors that are more aggressive because they do not depend on androgens for their growth.

Whatever the correct explanation turns out to be, concerns about the high incidence of aggressive cancers makes it inappro­priate to recommend finasteride for routine use as a cancer prevention agent.

14. Essay on Cancer Prevention: (Around 550 Words)

A Healthy Body Weight and Regular Physical Exercise can Reduce Cancer Risks :

It has been known for many years that individuals who are overweight have a higher-than-normal incidence of several types cancer, mainly uterine, breast, and colon cancers. Only recently has it become apparent that the impact of being overweight is much broader than this.

In 2003, the American Cancer Society published a study in which body weight and cancer death rates were tracked in more than 900,000 people for 16 years. The data revealed that obesity is linked to increased death rates for cancers of the uterus, breast, colon, esophagus, pancreas, kidney, gallbladder, ovary, liver, and prostate, as well as cancers of blood cells such as multiple myeloma and non-Hodgkin’s lymphoma.

To determine who was overweight, these studies estimated the amount of body fat each person carries using a formula based on height and weight called the Body Mass Index (BMI):

The linkage between cancer and excess body weight is especially troubling because a growing epidemic of obesity has been occurring in the United States since the early 1980s. By the year 2000, roughly 60% of U.S. adults were categorized as being overweight or obese, putting more than 100 million people at increased risk for dying of cancer (Figure 13).

Because the American Cancer Society study measured cancer death rates, its conclusions reflect the combined influence of body weight on both the risk of developing cancer and survival rates after diagnosis. How does excess body weight exert its negative influence on these events?

Several mechanisms are thought to be involved, but a central element appears to be the tendency of obesity to raise circulating levels of insulin, estrogen, and other growth-stimulating hormones. Such molecules can con­tribute to the promotion phase of carcinogenesis by stimulating cell proliferation and may also stimulate tumor growth after cancer has arisen.

There are two ways of avoiding the accumulation of excess body weight that leads to increased cancer risk. One is to eat a diet that does not contain too many calo­ries, and the other is to engage in regular physical exercise. Exercise plays an especially important role because its effects on cancer risk are not limited to main­taining a healthy body weight.

When individuals of the same exact weight are compared with one another, those who are physically active still have lower cancer rates than those who are inactive. One possible explanation is that individuals who exercise regularly tend to have more muscle tissue and less body fat than individuals of the same weight who do not exercise, and reduced levels of body fat are associated with hormonal and metabolic changes that may reduce cancer risks. Exercise-induced stimulation of immune function and antioxidant path­ways has also been reported, but the relevance of these changes (if any) to the development of cancer remains to be determined.

15. Essay on Cancer Prevention: (Around 450 Words)

Vaccines and Antibiotics are Useful for Preventing Cancers Caused by Viruses and Bacteria :

The importance of avoiding exposure to cancer-causing infectious agents—such as human papillomavirus, hepatitis B virus, hepatitis C virus, and the bacterium H. pylori. Complete avoidance, however, is extremely difficult because of the widespread prevalence of these infectious agents. It is therefore important to pursue approaches for preventing cancer from arising in people who have already been exposed.

One strategy is the development of vaccines that immunize against cancer-causing infectious agents. In the case of the hepatitis B virus, effective vaccines have been available since 1982.

Many countries now include hepatitis B vaccination in their routine childhood immunization programs, and reduced liver cancer rates have already been reported in immunized individuals. Developing a vaccine for hepatitis C has taken longer because the hepatitis C virus exhibits greater genetic variability, but candidate vaccines are currently being developed and evaluated.

Vaccination against human papillomavirus (HPV), the main cause of cervical cancer, is also being actively pursued. Creating a vaccine that protects against HPV is not a straightforward task because more than 100 different types of HPV exist and roughly a dozen have been implicated in the development of cancer. HPV 16 was the first to be pursued as a vaccine target because it is the most common strain of HPV in invasive cervical cancers, occurring in more than 50% of such tumors.

In 2002, results from the first successful trial of an HPV 16 vaccine were reported in a study involving more than 2300 women. The vaccine was found to be 100% effective in preventing HPV 16 infection and cervical cancer over a period of two years. Preliminary testing of another vaccine, which includes protection against HPV 18 as well as HPV 16, has also been successful, and it is anticipated that these vaccines will soon meet FDA requirements for general use.

Finally, H. pylori is one of the most common disease- causing microbes worldwide, infecting roughly two-thirds of the global population. Efforts to prevent stomach cancer caused by chronic infection with this bacterium are being pursued in two different ways. First, a vaccine designed to block persistent infection with H. pylori has been developed and is currently undergoing human testing.

In addition, the fact that H. pylori is a bacterium rather than a virus makes it susceptible to treatment with antibiotics. When antibiotics are administered to infected individuals early in the course of infection to rid them of H. pylori, the risk of stomach cancer is dramatically reduced.

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Essay on Cancer

List of essays on cancer, essay on cancer – introduction, types and conclusion (essay 1 – 150 words), essay on cancer (essay 2 – 250 words), essay on cancer – for school students (essay 3 – 300 words), essay on cancer – for medical students (essay 4 – 400 words), essay on cancer – for science students (essay 5 – 500 words), essay on cancer (essay 6 – 600 words), essay on cancer – written in english (essay 7 – 750 words), essay on cancer – for ias, civil services, upsc, ips and other competitive exams (essay 8 – 1000 words).

Cancer is a disease which is related to the abnormal growth of cells in a particular part of the body. Since the last decade, cancer has become one of the most feared diseases of all times, particularly due to the difficult treatment one has to undergo and the limitations of the treatment in curing this disease during later stages of cancer.

Audience: The below given essays are exclusively written for school and college students. Furthermore, those students preparing for IAS, IPS, UPSC, Civil Services and other competitive exams can also increase their knowledge by studying these essays.

Introduction:

Cancer is a group of more than 100 diseases that can develop in almost anywhere in the body. Cancer is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body.

Types of Cancer:

There are various types of cancer. They include:

1] Breast cancer: This is type of cancer that forms in the cells of the breast.

2] Prostate cancer: This is type of cancer that occurs in a man’s prostate. This is a small walnut sized gland that has the duty of producing seminal fluid.

3] Lung cancer: This is a type of cancer that begins in the lungs and this occurs mostly in people who smoke.

4] Leukemia: A cancer of blood forming tissues, hindering the body’s ability to fight infection.

Conclusion:

We have seen various types of cancer but the types of cancer we have are hundreds but we had mentioned just a few. Each type of cancer comes with various symptoms and various ways of curbing it.

Cancer is a disease that has been around for centuries, but it has never had such an impact on public health as it has now. Cancer is the increase in the number of cells in human beings at an abnormal rate. Doctors have been discussing the reasons behind this increase for the past fifty years. One is tempted to think that there are no reasons behind this occurrence and that it is just a natural phenomenon, people die all the time. Right?

The thing is that the number of cancer cases has increased in the past decades and a lot of this increase is attributed to the influence of different types of radiation. Even though most of the really dangerous substances (or sources of radiation) are not allowed near people. What else can be causing such an increase in cancer cases?

Some doctors have made a discovery regarding cancer that can really help us get rid of this problem. Following down the line of the argumentation presented in the famous “China Study” more doctors are advising their patients to change their diet because it can help  in their fight against cancer. Not only that but a proper diet can also be the best prevention.

When you are a student your metabolism is young so you do not feel the bad effect of your habits as much as older people do but as we age the side effects of our bad choices will become obvious. We can teach ourselves to listen to our bodies and to prevent cancer but to do that we, first of all, have to defeat our habits.

Cancer is uncontrolled and unchecked development of abnormal cells in a part of the body. Cancerous cells develop just like another cell in the body. They, however, keep growing and can form a mass then subsequently becomes tumors. Since cells are present in every part of our body, cancer can also grow in all parts of our body.

Causes of Cancer:

One great scientific mystery in our world is the cause of cancer. Scientists from all over have tried and failed in isolating any particular action, substance or environmental factors that can lead to cancer.

However, scientists all over the world agree that cancer is caused by substances known as carcinogens. These substances are introduced to the body when we are exposed to or consume materials containing them. One of the confirmed sources of carcinogens is exposure to radiation from x-ray machines.

Cancer Treatment:

There are various ways to treat a person infected with cancer. These modes of treatment are chosen depending on the type of cancer, the stage of development and the health peculiarities of the cancer patient. In other cases, several modes of treatment are combined to treat a single patient.

Some of the modes of treating cancer are in fly highlighted below:

1. Surgery to remove Cancerous tumors from the body.

2. Radiation therapy to reduce the growth of cells.

3. Chemotherapy for destroying cancer cells.

4. Stem cell transplant.

Prevention of Cancer:

Just as there are no agreed actions, materials and exposure that causes cancer, there are no generally accepted means of preventing cancer. However, there are certain habits that can limit a person’s exposure.

Some of them are highlighted below:

1. Healthy environment and diet.

2. Reduction of exposure from the sun.

3. Keep your weight low.

4. Avoid the use of tobacco.

Early detection of cancer has been hailed as the most potent way of treating this menace. Though scientists are still in the business of searching for a cure, we as humans can prevent cancer by regular medical check-ups.

Cancer is one of the second largest fatal illnesses across the world. One of the horrific words a human being can listen to is being diagnosed with Cancer. The word Cancer brings alarm and anxiety to the listener. Cancer is the abnormal growth of cells in one part of the body which can even spread to other parts if not treated at an early stage. Neoplasms or tumour are the subset of these abnormally grown-up cells which often results in a mass or lump.

What causes Cancer?

Those agents which cause cancer are termed as Carcinogens . These can be classified into physical, chemical and biological. Physical Carcinogens include ultra violet and other ionizing radiations. Food adulterants such as aflatoxin, tobacco smoke, drinking water contaminant such as Arsenic, asbestos etc., are termed as Chemical Carcinogens. Viruses, Bacteria and other parasites which cause infections and eventually lead to Cancer are categorized under Biological Carcinogens. Ageing also causes cancer as the risk of the cellular repair mechanism weakens as we age.

Significant Symptoms of Cancer:

Some of the major symptoms of cancer include unexplained weight loss, extreme fatigue, persistent sores that do not heal, changes in the bladder and bowel movements, odd bleeding and discharges, change in voice due to cancer indication in larynx and lumps and bumps on the skin.

Preventive Measures:

Some of the risk factors which needs to be addressed to prevent cancer may include avoidance of tobacco, being overweight or obese, unhealthy eating with less vegetables and greens, physical in-activity, avoiding pollution etc. Apart from the mentioned, vaccination against HPV and Hepatitis B Virus, controlling hazards while at work, reducing exposure to ultra violet and ionizing radiation etc., can help prevent being infected by Cancer.

Assessing the type of cancer and the stage is very important because every cancer type has a different pattern of treatment from surgery, radiotherapy and chemotherapy . The treatment that is used to relieve the cancer patient from their pain and enhance the quality of life for the patients and their families is termed as Palliative care.

World Health Organization has partnered with UNO and other non-profit organizations to ensure every country is being made aware of the non-communicable diseases and the prevention of cancer and its control. Insights to develop Centers of Excellence to provide quality treatments and to conduct research on the carcinogenesis should be provided to governments and to help the people.

The abnormal cell growth in our body which spreads to other parts as well is what is termed as cancer. Around four lakh of people in India are known to be affected by this disease every year. More so, around half of them are not able to survive as they are usually detected in the last stages of cancer. Hence it is all the more important to educate the people about this disease and its symptoms so that it can be detected early and the lives of the people suffering from it can be saved.

Cancer can affect any body part. The part that is affected gives it the name, for instance, lung cancer which affects the lungs, skin cancer in which the skin is affected and so on. However, we can broadly divide cancer into four types. The first one is Sarcoma which is known to affect the blood vessels, bones, muscles cartilages and connective tissues. The second type of cancer is Carcinoma which affects the internal organs of the body or the skin. The third type is the Lymphoma. This cancer affects the lymph glands and the lymph nodes. The last type in which cancer can be categorised is Leukaemia which largely affects the parts forming blood such as the bone marrow.

Symptoms of Cancer:

Although no particular cause is known to trigger this disease, some activities have been associated as the cause of different types of cancer. The first and foremost is smoking. Excess smoking affects the entire respiratory system thereby leading to the onset of lung cancer. More so chewing tobacco is also attributed to giving rise to mouth and throat cancer. Similarly, alcohol is attributed to be the cause of stomach, liver and gallbladder cancer. Summarising it, all the ill habits of society and urbanisation have been attributed to this disease. Even radiations coming from X-ray machines can prove harmful and lead to cancer. That is why there are proper laws an protection in place when exposing people to these harmful radiations.

Treatments Available:

If detected in early stages, cancer can surely be curable. Surgery is one of the primary steps of curing this disease. If required, doctors remove the body part affected such as the uterus, gallbladder or the breast. Thereafter, through radiotherapy, the cancerous cells on the other affected parts of the body are killed so that they don’t spread to other parts. Chemotherapy is done using the strong chemical in order to kill the cancerous cells. Other methods such as tumour suppressing genes are used in different types of cancer as may be the need advised by the doctors. Whatever the method, it is extremely difficult to go through the pain and social stigma such as loss hair which comes alongside the treatment of cancer.

Living with this Disease:

It is indeed very difficult to live with this disease as not only this disease is not fully curable but the treatment is so tough that it scares even the toughest of individuals. We, as a society, must support the people suffering from cancer and help in their difficult times. We must not discriminate them and must understand that is already suffering a lot and must not do anything which further aggravates their sufferings.

Cancer is a severe disease in which there is abnormal growth of cell that spreads around the human body. Many people in the world are struggling with this disease. Consistently around 10 million cases are analyzed. These number of cases are expected to increase around 20 million by 2020. It turns into the most widely recognized reasons for death. Due to abnormal cell growth, it develops & affects the overall body weight. Prolonged cough and abnormal bleeding are some symptoms of this severe disease. The developed abnormal cells first make their impact on organs then slowly moved as poison. Cancer disease can be identified in the beginning periods. The medical professionals are still trying to catch this disease.

One of the main causes of cancer is smoking. Other causes include tobacco, consumption of alcohol, obesity, lack of physical activities, exposure to UV radiations, etc. Age factor and changes in genes are yet other factors that cause cancer.

Cancer has different types which can be divided into various forms:

i. Skin Cancer:

It is the most common type of cancer which can be seen in many people. Every year more than 1 million people are affected by skin cancer. Skin cancer happens due to the overexposure from the sun. The thicker ozone layers directly harms our skin, which increases the chances of skin cancer.

ii. Lung Cancer:

This type of cancer is related to the cells inside the lungs. The symptoms of this type of cancer are chest pain & sudden weight loss. It is also known as lung carcinoma. As a process of metastasis, the growth of abnormal cell growth spread inside the lungs. Smoking is a fundamental driver of Lung cases.

iii. Kidney Cancer:

Another name of kidney cancer is renal cancer. Renal Cell Carcinoma and Transitional Cell Carcinoma are the types of kidney cancer. This development of cancer happens after the age of 40 years. Smoking can twofold the danger of kidney malignant growth.

iv. Leukemia:

This cancer starts developing in the bone marrow, which leads to a high number of abnormal white cells. Acute myeloid leukemia or acute lymphocytic leukemia are the sorts of leukemia. Chemotherapy or radiation therapy can be used as the treatment for Leukemia.

Cancer Staging:

It is important to understand the staging factor of this severe disease. Diagnosis of cancer in early stages helps to tackle this disease by proper treatments. During the initial stages of cancer, proper surgeries or radiotherapy can help to overcome cancer. When the broken cancer cells move to other parts of the human body, then advance treatment is suggested by the professionals. But when a patient is in the final stages of cancer, he needs a treatment which covers his whole body. Chemotherapy is a therapy which is used to circulate the bloodstream. Professional doctors use various test techniques to identify the stages of cancer. Stages are used to describe the severity of cancer.

In the initial stage, cancer can be prevented through medication, proper surgeries and light treatment. In the advance stages of cancer, chemotherapy and radiation therapy is useful. Above all, the best way to keep cancer away is to stay away from smoking and tobacco, eat healthy food and a lot of green vegetables, and do some physical exercise daily.

It is very difficult for a cancer patient to fight with the final stages of cancer. To deal with this severe problem cancer symptoms should never be ignored. More than 70% of cases are seen only due to smoking. At every stage, it is essential that everyone must adopt a healthy diet plan & exercise daily to prevent this disease. A person who has a good and healthy lifestyle can fight with cancer more strongly.

Current trends in global health mention cancer. Cancer is currently one of the leading causes of death globally. It is an illness in which abnormal cell growth develops and affects parts of the human body as it advances, it has the potential to spread from one part of the body to the other. It is a chronic illness that imposes a great economic burden on a nation because its management is costly. Cancer occurs in different parts of the body and are classified according to where it has affected. In India, men are mostly acted by lung, oral, lip and neck cancers whereas women are affected by cervical, breast and ovarian cancer. The detection procedure varies with the type of cancer while the treatment varies with the stage of the cancer progression. Mostly early stages of cancer have better prognosis compared to late stages of cancer.

There are modifiable and non-modifiable factors that predispose an individual to cancer. Non modifiable factors include age and genetics. With an increase in age, the rate of cancer incidence increases. The genetic predisposition to cancer increases the incidences of suffering the disease. Modifiable factors include lifestyle habits like drinking and smoking tobacco which increase the incidences of lung, oral, esophageal among other cancers. Diet is also a predisposing factor especially one that is less in vitamin supplements.

Physical inactivity and obesity predispose to cancers of the colon, breast and others. Sexual activity in women with multiple sexual partners predisposes them to cervical cancer due to the transmission of HPV (Human Papilloma Virus). The environment also predisposes to cancer because of the chemicals, radicals and radiations that interact with human beings.

Detection of Cancer:

The detection varies with the type of cancer and so screening is done for each type differently. It is advisable that people get regular checkups of the whole body so that early detection facilitates effective and curative treatment. Screening of cancer is done using detailed examination of the physique, laboratory and histology tests, radiological and magnetic imaging techniques among other methods.

The campaigns against cancer advocate for early detection by teaching the public on the early signs of cancer. In breast cancer awareness for example, the public is made aware of physical examination of the breast and if they detect any abnormal growth or lump, they are to seek further investigation. Early detection is important because it results in successful treatment. In the detection, the cancer staging is done, which is usually four stages, stage one, two, three and four. Stage one has the best prognosis whereas stage four has the poorest prognosis.

Treatment of Cancer:

Once cancer is detected, a range of treatment options is provided. Treatment depends on the types of cancer and the staging. It can be treated by surgery whereby excision of the abnormal growth is done. Surgery is done for non-hematological cancers and those that have not metastasized to other parts of the body. An example of surgery is mastectomy to treat breast cancer.

Chemotherapy is another treatment option that involves the administration of anticancer medication that eliminate the abnormal cells in the body. Another treatment option is radiation therapy that uses ionizing radiations to destroy cancer cells. Radiation is also used to make tumors small. It is used to treat solid tumors and it depends on the sensitivity of the tumor to the radiations. It is targeted at the nucleic acid destruction in the tumor cells.

Consequences of Cancer:

Cancer is a chronic illness that could result in very serious consequences even with treatment. Cachexia is the extreme wasting of the body that causes death in cancer patients. Economic burden to both the individual and the nation is experienced in cancer treatment because the treatment modalities are costly. The economic burden results in decline of the nation’s economy and increased healthcare costs to the population.

Mental illnesses result from cancer because it is a terminal illness and most patients become mentally unstable upon diagnosis. The quality of health is affected in a country when there is high incidences of cancer and the performance is greatly affected, which cause poverty and economic crisis for individuals.

Cancer is a serious illness that impacts the lives of people and the nation negatively. It is evident that cancer has diverse treatment options but the problem is that people do not go for checkups. Checkups are important in early detection, which usually results in successful treatment and less burden of cancer in a nation and in individuals.

Cancer is basically an agglomeration of various diseases that involves the abnormal growth of cells with the ability to spread or invade other body parts. Cancers are quite different from benign tumours in that the latter does not spread or invade other body parts. Some of the many symptoms and signs of cancer include abnormal bleeding, a lump, weight loss that is unusual, prolonged cough and bowel movement change. Even though these listed symptoms and signs of cancer, they might be caused by other things so it is necessary to be diagnosed. Today, we have more than 100 various kinds of cancer that affect us humans.

History of Cancer:

It is believed that cancer has been in existence for a majority if not all of the history of man. Breast cancer was the first form of cancer that was recorded and this happened around 1600 BC in Egypt. Between 460 BC and 370 BC, Hippocrates spent time analysing various types of cancer and referred to them as crayfish or crab. The name was as a result of the crab-like look of the malignant tumour and the lateral extension of the distended veins and tumours.

Factors Causing Cancer:

It has been discovered that the major cause of deaths as a result of cancer is the use of tobacco and it accounts for about 22 percent of the total number of deaths due to cancer. Poor diet, obesity, excessive alcohol consumption and a lack of exercise and physical activities accounts for another 10 percent of deaths caused by cancer. Some other causes and factors that contribute to cancer include environmental pollutants, ionizing radiation exposure and certain infections.

In most developing countries, infections like hepatitis B, Helicobacter pylori, papillomavirus infection of humans, Hepatitis C, HIV and Epstein Barr contribute to fifteen percent of all cancers. All of the factors listed above change the cell genes. There are always a lot of genetic changes before the development of cancer. About 10% of all cancers are as a result of genetic defects that are inherited from a parent. Asides the symptoms and signs that are used to detect cancer, screening tests are also a good way of detecting cancer. Cancer is normally thoroughly investigated using medical imaging; it is then confirmed through biopsy.

Development of Cancer:

A tumour or neoplasm is a collection of cells which have gone through growth that is not regulated and most times form a lump or mass. Every tumour cell exhibits the six important characters that are necessary for the production of the malignant tumour.

The six characteristics are:

1. Cell division and growth without all the signals that are proper.

2. Continuous division and growth even though the signals given are contrary.

3. Cell death that is usually programmed is avoided.

4. The divisions of the cell are quite limitless in number.

5. The construction of blood vessel is promoted.

6. The tissues are invaded and metastases are formed.

Cancer Prevention:

The prevention of a lot of cancers can be ensured by trying to maintain a weight that is healthy, not smoking, consuming a lot of whole grains, fruits and vegetable, avoiding the consumption of a lot of alcohol, reduction in the amount of red and processed meat that is consumed, getting vaccinated against some infectious diseases and the avoidance of too much exposure to sunlight. It is sometimes useful that there is early detection in cases of colorectal and cervical cancer and this can be achieved through screening. The usefulness of breast cancer screening is highly controversial.

The treatment of cancer is usually done by combining surgery, radiation therapy, targeted therapy and chemotherapy. A very important element of care is the management of symptoms and pain. In cases of advanced disease, palliative care is of utmost importance. The extent of the disease at the commencement of treatment and also the form of cancer that is involved go a long way to determine the odds of survival. Using the adopted survival rate at five years, children that were under the age of 15 when they were diagnosed have an average rate of survival of 80% in most developed countries. In the US, the average rate of survival for the five year period is 66%.

90.5 million  people were living with different cancers in 2015. It has been reported that every year, close to 15 million reports of new cancer cases are filed. These do not include the cases of skin cancer. Cancer results in more than eight million deaths every year which is about 15.7% of the total number of deaths every year.

In males, prostate cancer, lung cancer, stomach cancer and colorectal cancer are the most widespread cancer types. In females, colorectal cancer, breast cancer, cervical cancer and lung cancer are the most widespread cancer types. Apart from melanoma, if we include skin cancer in the amount of new cases of cancer every year, it is going to be 40% of the total number of cases.

Brain tumours and lymphoblastic leukemia that is acute are the most widespread cancer types in children but in Africa, lymphoma that is no-Hodgkin is the most widespread. The total number of children that are under the age of 15 that ended up being diagnosed with one type of cancer or the other in 2012 is around 165,000.

With an increase in age, it has been seen that the risk of getting cancer also increases significantly and the number and occurrence of cases of cancer in developed countries in more than the number and occurrence of cancer cases in other countries. The change in lifestyle and increase in the number of people living to a very old age in countries that are developing contributes to the increase in the rate of the occurrence of cancer. Cancer is believed to have a financial cost of up to 1.16 trillion dollars every year.

Cancer can be extremely dangerous when it is not discovered early and when adequate and proper care and attention is not given to the treatment. Therefore it is very important to go for regularly screening to find out if there is need for caution or treatment.

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Can aspirin help protect against colorectal cancers?

A new study details how a daily dose could prevent or delay the progression of the world’s third most common type of cancer.

Aspirin is well known for its ability to ease pain from muscle aches and headaches; it reduces fevers; and low doses can thin blood, reducing the chance of clots that cause strokes and heart attacks. Now a new study suggests it may also play a role in colorectal cancer prevention.

Colorectal cancer, a cancer of either the large intestine or rectum, is the third most common type of cancer, and the second most common cause of death from cancer , worldwide. There were 1.9 million new cases diagnosed across the globe in 2020, according to the World Health Organization, and these numbers are expected to grow. In the United States, the rates of colorectal cancers have been rising in people younger than age 50 since the 1990s, which includes more young people dying from the disease, according to the National Cancer Institute .  

Now a new study published in the journal Cancer shows that colorectal cancer patients who took a daily dose of aspirin had a lower rate of metastasis to the lymph nodes and stronger immune response to their tumors. The research suggests that aspirin may be boosting the ability of the immune system to hunt for cancer cells.  

“It is a rather unexpected effect, because aspirin is mainly used as an anti-inflammatory drug,” says Marco Scarpa, a researcher at the University of Padova, and one of the authors of the study. As Scarpa notes, this study suggests that aspirin may be playing a slightly different role by stimulating the immune system’s surveillance response, which can then prevent or delay the progression of colorectal cancer.  

Your immune system is always surveilling the body for cells that just aren’t right. When they find such cancer cells, they will kill them just as they would kill invading bacteria or viruses, says Cindy Kin , a surgeon at Stanford University, who specializes in colon and rectal surgery.  

“The data about aspirin and cancer is really evolving,” says Maen Abdelrahim , an oncologist at Houston Methodist Hospital, who specializes in treating colorectal cancers. However, there are still a lot of unanswered questions about how aspirin can prevent and delay the progression of these cancers, as well as which subset of patients would benefit from a daily aspirin.  

( Colon cancer is rising among young adults. Here are signs to watch for. )

People who take a consistent use of aspirin have a lower risk of colorectal cancer, “but it has to be balanced with the risks,” which includes the possibility of bleeding in the gastrointestinal tract, says Jeff Meyerhardt , an oncologist and co-director of the Colon and Rectal Cancer Center at the Dana-Farber Cancer Institute, in Boston.  

Aspirin protects against colorectal cancer

There are several studies that suggest a link between aspirin and colorectal cancer prevention and delay. However, the mechanism by which aspirin does this is still unknown. That makes it hard to predict which patients will benefit the most.  

In a 2020 meta-analysis , which analyzed the results of 45 observational studies, researchers found that regular aspirin use was associated with less incidence of colorectal cancer.  

A low dose, between 75 and 100 milligrams, was associated with a 10 percent reduction in the risk of developing colorectal cancer; a regular dose of 325 milligrams was associated with a 35 percent decline.  

Other studies have shown a link between daily aspirin and a delayed progression , including a lower risk of dying in patients who had already been diagnosed with colorectal cancer.  

“What has been seen in multiple studies for colorectal cancers is that having a more robust immune reaction does seem to have a better outcome,” Meyerhardt says. “This is looking at how aspirin may interact with that.”  

Study suggests mechanism

In the study, researchers obtained tissue samples from 238 patients who had undergone surgery for the colorectal cancers. Of these patients, 12 percent were taking a daily low dose of aspirin for the prevention of heart disease. When compared to patients who were not taking aspirin, the researchers found a lower rate of metastasis to the lymph nodes, and higher numbers of immune cells that had infiltrated the tumors.  

This higher level of infiltration is thought to be linked to slower cancer progression—including the lower rate of spread to the lymph nodes—by allowing immune cells to enter the tumor mass and fight the cancerous cells more effectively.  

( Why is stomach cancer rising in young women? )

The researchers also found higher levels of immune markers that are responsible for triggering the immune system surveillance response. “It’s boosting the immune system, and it’s helping the immune system inside the tumor,” Abdelrahim says.  

In recent years, the immune system’s role in protecting against the development of cancer has become recognized.  

Patients with suppressed immune systems are at higher risk for developing cancers , compared to patients with a fully functional immune system. As these results suggest, aspirin may increase the vigilance of the immune system when it comes to the detection of colorectal cancers.  

“Your immune system is doing all of these things in the background, that you’re not even aware of,” Kin says. “It’s not just the tumor’s behavior and how aggressive it’s going to be, but it’s your body versus the tumor.”  

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3 high-fiber dinner recipes to help prevent colon cancer — which is rising in young people — from a cancer dietitian

• Colorectal cancer rates in younger people have been rising for the past two decades. 
• Eating fiber-filled whole grains and avoiding saturated fats can help reduce the risk, research suggests.
• Meredy Birdi, a cancer dietician, shared three dinner recipes to help prevent colorectal cancer.

Colon cancer cases are rising in younger people, and experts don't yet know why. But certain lifestyle factors are thought to decrease the risk of developing the disease.

Over the past two decades, deaths from colon cancer in people under 55 have steadily risen by around 2% a year, according to the American Cancer Society. It is now the deadliest cancer for men under 50 in the US, and the second deadliest for women the same age. In 2020, around $24.3 billion was spent on treating colorectal cancer, accounting for 12.6% of all US cancer treatment costs, according to the ACS.

Alcohol, a lack of physical activity, and eating a traditional Western diet can all increase colon cancer risk, Meredy Birdi , a cancer dietitian based in London, told Business Insider. This means a diet high in ultra-processed foods , refined carbohydrates such as white bread, pizza, and cookies, and saturated fats found in fatty meats and butter, that's also lacking in fiber, she said.

Fiber comes from plants such as whole grains, fruits and vegetables, legumes, nuts, and seeds, and there's strong evidence to suggest that it lowers colon cancer risk. It feeds the good bacteria in the gut , Birdi said, which protect the gut lining. It also acts as nature's broom, sweeping out toxins, she said.

Birdi said that people should aim to eat plant-based 75% of the time. "It's about balance. So nobody needs to worry about the occasional things that they do," she said.

She shared three fiber-filled dinner recipes that could help prevent colon cancer with BI.

Bean chili with brown rice

Beans are an excellent source of fiber as well as plant-based protein. They're a good substitute for red meat, which has been linked to an increased risk of colon cancer, according to the World Cancer Research Fund International, a cancer-prevention organization focused on how diet, weight, and physical activity can affect cancer survival rates.

Related stories

A bean chili with vegetables and brown rice is a simple, high-fiber dinner that contains legumes, whole grains, and vegetables, Birdi said. She recommended this recipe shared by the WCRF, but specified that it's best to use olive oil, a source of healthy unsaturated fats .

It takes 25 minutes to make, and it contains six portions of vegetables.

Vegan jambalaya

Jambalaya is a one-pot rice dish that originated in Louisana. It's typically made with meat or seafood, but if you make a vegan version, it becomes a higher-fiber, nutrient-dense dish.

Birdi recommended this recipe , which substitutes animal products for butter beans. The recipe also calls for brown rice, which contains more fiber than its white counterpart.

You'll need garlic, chopped tomatoes, onion, celery, yellow pepper, herbs, spices, and vegetable stock. It cooks in 35 minutes.

Turkey and chickpea curry

Another delicious dinner option is a turkey and chickpea curry, she said. It's high in protein and fiber.

Chickpeas contain nearly 15 grams of protein and 12 grams of fiber per cup, which is close to half the recommended daily dose of fiber, while turkey is a lean source of protein.

Birdi uses this recipe but recommends using olive oil instead of vegetable oil, as the recipe states. Extra virgin olive oil , in particular, contains more healthy fats and antioxidants than vegetable oil, according to Healthline .

Watch: US vs UK vs Japan vs India McDonald's | Food Wars

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How does aspirin help prevent colorectal cancer development and progression?

Long-term daily use of aspirin can help to prevent the development and progression of colorectal cancer, but the mechanisms involved have been unclear. New research has revealed that aspirin may exert these protective effects by boosting certain aspects of the body's immune response against cancer cells. The findings are published in Cancer .

To investigate the effects of aspirin (a nonsteroidal anti-inflammatory drug) on colorectal cancer , investigators in Italy obtained tissue samples from 238 patients who underwent surgery for colorectal cancer in 2015–2019, 12% of whom were aspirin users.

Patients were enrolled in the METACCRE section of the IMMUNOlogical microenvironment in the REctal Adenocarcinoma Treatment (IMMUNOREACT 8) multicenter observational study. The study was mainly carried out at the University Hospital of Padova.

Compared with tissue samples from patients who did not use aspirin, samples from aspirin users showed less cancer spread to the lymph nodes and higher infiltration of immune cells into tumors. In analyses of colorectal cancer cells in the lab, exposing the cells to aspirin caused increased expression of a protein called CD80 on certain immune cells, which enhanced the capacity of the cells to alert other immune cells of the presence of tumor-associated proteins.

Supporting this finding, the researchers found that in patients with rectal cancer, aspirin users had higher CD80 expression in healthy rectal tissue, suggesting a pro-immune surveillance effect of aspirin.

"Our study shows a complementary mechanism of cancer prevention or therapy with aspirin besides its classical drug mechanism involving inhibition of inflammation," said principal investigator Marco Scarpa MD, Ph.D., of the University of Padova.

"Aspirin is absorbed in the colon by passive diffusion to a significant degree. Its absorption is linear and depends on concentration along the bowel, and in the rectum, the concentration of orally administered aspirin can be much lower than in the rest of the colon.

"Thus, if we want to take advantage of its effects against colorectal cancer, we should think of how to guarantee that aspirin reaches the colorectal tract in adequate doses to be effective."

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The beautiful, sunny weather we’ve been experiencing in the Tampa Bay area recently has been a great tease for the summer and a great reminder to start thinking about our skin’s health as we approach summer. Spending time in the sun is crucial to our health, but it’s important to remember to keep your skin’s health top of mind.

According to the Skin Cancer Foundation, 1 in 5 Americans will face a battle with skin cancer by the time they reach age 70. While this statistic is daunting, early detection can play a crucial role in combating and surviving skin cancer. Melanoma is the most dangerous form of skin cancer, but when it’s detected early enough, the survival rates are extremely high. Melanoma can occur in all skin types, which is why I strongly encourage everyone, regardless of age, gender or race, to get skin checks on an annual basis.

The significance of routine skin checks can’t be overstated in the fight against melanoma. These annual checks allow clinicians to acquaint themselves with their patients’ skin profiles and promptly identify any suspicious moles, growths or spots for further evaluation or removal.

Melanoma Monday, which takes place the first Monday of every May, is coming soon on May 6. The day serves as a reminder about the dangers of skin cancer but also to encourage skin checks. I encourage you to schedule a skin check with a clinician and be on the lookout for any clinics that offer free skin checks on Melanoma Monday, like ours at Advanced Dermatology and Cosmetic Surgery.

So, what can you expect at a skin check? The process is fast, painless and straightforward. Your clinician will meticulously examine your skin, noting any moles, spots or growths. Then, depending on what the clinician ends up finding, they may advise regular monitoring for changes in a mole or opt for its immediate removal, sending it off for analysis in a laboratory.

The process doesn’t take much longer than around 10 minutes, but that extremely brief period of time has the potential to save lives by detecting melanoma at its earliest stages. Considering melanoma’s status as the deadliest form of skin cancer, this minimal investment of time and effort is undoubtedly worthwhile. Skin checks aren’t just routine appointments. They’re proactive measures in safeguarding your health and well-being. Not nearly enough people prioritize their skin health and take the necessary steps to combat skin cancer effectively, which is why I believe this message is so important.

Beyond the imperative of early detection lies the crucial aspect of understanding risk factors and preventative measures against skin cancer. While fair-skinned individuals are often more susceptible to skin cancer due to lower levels of melanin, no one is immune, regardless of skin color or ethnicity. However, individuals with a history of excessive sun exposure, blistering sunburns or a family history of skin cancer are at heightened risk and should be particularly vigilant.

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Sun protection is also extremely important in reducing the risk of skin cancer. There are many ways to protect yourself from the sun, including applying sunscreen with a high SPF regularly, seeking shade during peak sun hours, wearing protective clothing and using broad-brimmed hats and sunglasses. It’s also important to avoid tanning beds and other sources of artificial UV radiation, as they significantly increase the risk of skin cancer.

Education is key in fostering a culture of skin cancer prevention. Promoting awareness about the importance of sun safety practices, early detection and regular skin checks is essential in empowering people to take proactive steps to protect their skin health. Schools, workplaces and community organizations can play a pivotal role in making sure this information gets out to the public. It’s ultimately a group effort that must be taken seriously if we want to reduce rates of melanoma.

Skin checks have the power to save lives. They are one of the most important tools we have in the fight against melanoma and other forms of skin cancer. Regardless of age, gender or skin type, prioritizing skin checks can help make significant strides in reducing the frequency of melanoma. I highly encourage anyone reading this to take the first step and call a dermatology office to get a skin check scheduled.

Dr. Lisa Nyanda is a dermatologist with Advanced Dermatology and Cosmetic Surgery. A specialist in pediatrics and general and cosmetic dermatology, she practices in the Tampa Bay area and is a fellow of the American Academy of Dermatology and the American Academy of Pediatrics.

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How to Thrive as You Age

A cheap drug may slow down aging. a study will determine if it works.

Allison Aubrey

A drug taken by millions of people to control diabetes may do more than lower blood sugar.

Research suggests metformin has anti-inflammatory effects that could help protect against common age-related diseases including heart disease, cancer, and cognitive decline.

Scientists who study the biology of aging have designed a clinical study, known as The TAME Trial, to test whether metformin can help prevent these diseases and promote a longer healthspan in healthy, older adults.

Michael Cantor, an attorney, and his wife Shari Cantor , the mayor of West Hartford, Connecticut both take metformin. "I tell all my friends about it," Michael Cantor says. "We all want to live a little longer, high-quality life if we can," he says.

Michael Cantor started on metformin about a decade ago when his weight and blood sugar were creeping up. Shari Cantor began taking metformin during the pandemic after she read that it may help protect against serious infections.

Shari and Michael Cantor both take metformin. They are both in their mid-60s and say they feel healthy and full of energy. Theresa Oberst/Michael Cantor hide caption

Shari and Michael Cantor both take metformin. They are both in their mid-60s and say they feel healthy and full of energy.

The Cantors are in their mid-60s and both say they feel healthy and have lots of energy. Both noticed improvements in their digestive systems – feeling more "regular" after they started on the drug,

Metformin costs less than a dollar a day, and depending on insurance, many people pay no out-of-pocket costs for the drug.

"I don't know if metformin increases lifespan in people, but the evidence that exists suggests that it very well might," says Steven Austad , a senior scientific advisor at the American Federation for Aging Research who studies the biology of aging.

An old drug with surprising benefits

Metformin was first used to treat diabetes in the 1950s in France. The drug is a derivative of guanidine , a compound found in Goat's Rue, an herbal medicine long used in Europe.

The FDA approved metformin for the treatment of type 2 diabetes in the U.S. in the 1990s. Since then, researchers have documented several surprises, including a reduced risk of cancer. "That was a bit of a shock," Austad says. A meta-analysis that included data from dozens of studies, found people who took metformin had a lower risk of several types of cancers , including gastrointestinal, urologic and blood cancers.

Austad also points to a British study that found a lower risk of dementia and mild cognitive decline among people with type 2 diabetes taking metformin. In addition, there's research pointing to improved cardiovascular outcomes in people who take metformin including a reduced risk of cardiovascular death .

As promising as this sounds, Austad says most of the evidence is observational, pointing only to an association between metformin and the reduced risk. The evidence stops short of proving cause and effect. Also, it's unknown if the benefits documented in people with diabetes will also reduce the risk of age-related diseases in healthy, older adults.

"That's what we need to figure out," says Steve Kritchevsky , a professor of gerontology at Wake Forest School of Medicine, who is a lead investigator for the Tame Trial.

The goal is to better understand the mechanisms and pathways by which metformin works in the body. For instance, researchers are looking at how the drug may help improve energy in the cells by stimulating autophagy, which is the process of clearing out or recycling damaged bits inside cells.

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Researchers also want to know more about how metformin can help reduce inflammation and oxidative stress, which may slow biological aging.

"When there's an excess of oxidative stress, it will damage the cell. And that accumulation of damage is essentially what aging is," Kritchevsky explains.

When the forces that are damaging cells are running faster than the forces that are repairing or replacing cells, that's aging, Kritchevsky says. And it's possible that drugs like metformin could slow this process down.

By targeting the biology of aging, the hope is to prevent or delay multiple diseases, says Dr. Nir Barzilai of Albert Einstein College of Medicine, who leads the effort to get the trial started.

The ultimate in preventative medicine

Back in 2015, Austad and a bunch of aging researchers began pushing for a clinical trial.

"A bunch of us went to the FDA to ask them to approve a trial for metformin,' Austad recalls, and the agency was receptive. "If you could help prevent multiple problems at the same time, like we think metformin may do, then that's almost the ultimate in preventative medicine," Austad says.

The aim is to enroll 3,000 people between the ages of 65 and 79 for a six-year trial. But Dr. Barzilai says it's been slow going to get it funded. "The main obstacle with funding this study is that metformin is a generic drug, so no pharmaceutical company is standing to make money," he says.

Barzilai has turned to philanthropists and foundations, and has some pledges. The National Institute on Aging, part of the National Institutes of Health, set aside about $5 million for the research, but that's not enough to pay for the study which is estimated to cost between $45 and $70 million.

The frustration over the lack of funding is that if the trial points to protective effects, millions of people could benefit. "It's something that everybody will be able to afford," Barzilai says.

Currently the FDA doesn't recognize aging as a disease to treat, but the researchers hope this would usher in a paradigm shift — from treating each age-related medical condition separately, to treating these conditions together, by targeting aging itself.

For now, metformin is only approved to treat type 2 diabetes in the U.S., but doctors can prescribe it off-label for conditions other than its approved use .

Michael and Shari Cantor's doctors were comfortable prescribing it to them, given the drug's long history of safety and the possible benefits in delaying age-related disease.

"I walk a lot, I hike, and at 65 I have a lot of energy," Michael Cantor says. I feel like the metformin helps," he says. He and Shari say they have not experienced any negative side effects.

Research shows a small percentage of people who take metformin experience GI distress that makes the drug intolerable. And, some people develop a b12 vitamin deficiency. One study found people over the age of 65 who take metformin may have a harder time building new muscle.

Millions of women are 'under-muscled.' These foods help build strength

"There's some evidence that people who exercise who are on metformin have less gain in muscle mass, says Dr. Eric Verdin , President of the Buck Institute for Research on Aging. That could be a concern for people who are under-muscled .

But Verdin says it may be possible to repurpose metformin in other ways "There are a number of companies that are exploring metformin in combination with other drugs," he says. He points to research underway to combine metformin with a drug called galantamine for the treatment of sarcopenia , which is the medical term for age-related muscle loss. Sarcopenia affects millions of older people, especially women .

The science of testing drugs to target aging is rapidly advancing, and metformin isn't the only medicine that may treat the underlying biology.

"Nobody thinks this is the be all and end all of drugs that target aging," Austad says. He says data from the clinical trial could stimulate investment by the big pharmaceutical companies in this area. "They may come up with much better drugs," he says.

Michael Cantor knows there's no guarantee with metformin. "Maybe it doesn't do what we think it does in terms of longevity, but it's certainly not going to do me any harm," he says.

Cantor's father had his first heart attack at 51. He says he wants to do all he can to prevent disease and live a healthy life, and he thinks Metformin is one tool that may help.

For now, Dr. Barzilai says the metformin clinical trial can get underway when the money comes in.

7 habits to live a healthier life, inspired by the world's longest-lived communities

This story was edited by Jane Greenhalgh

Alabama.com: How a new self-test for HPV could be a game changer

The University of Cincinnati's Leeya Pinder was featured in an Alabama.com article about how self-testing for HPV could make preventative care more accessible to those facing the most barriers.

To help close the gap in access to screening for cervical cancer, the National Cancer Institute has launched the Cervical Cancer ‘Last Mile’ Initiative, a public-private partnership working to provide evidence on the effectiveness and accuracy of self-testing for HPV. 

Part of this initiative is the SHIP trial (Self-collection for HPV testing to Improve Cervical Cancer Prevention). The University of Cincinnati Cancer Center is one of 25 SHIP trial sites across the country testing whether samples self-collected by patients for HPV testing are as accurate and effective as clinic-collected samples. 

“It really gives people the opportunity to just do a vaginal swab or a cervico-vaginal swab so that they can get tested for high-risk HPV, which is usually the driver of cervical precancer and cervical cancer,” said Pinder, MD, a University of Cincinnati Cancer Center member and associate professor in the UC College of Medicine Department of Obstetrics and Gynecology, Division of Gynecologic Oncology. “What we’ve been trying to do over the last several years is prove that women can actually do HPV testing on their own.”

Previous research has shown self-testing methods are effective, especially for certain underscreened populations.

“Those populations include those who sometimes struggle with substance abuse, sometimes have a history of trauma or other kinds of abuse, those that are concerned about their immigration status or actually, many things,” she said. “These are reaching the people who for whatever reason do not have great access to a health care provider to get their cervical cancer screening.”

Read the Alabama.com story , originally published on Reckon .

Read more about the SHIP trial.

Featured photo at top of HPV test form. Photo/iStock/Sefa Ozel.

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Guest Essay

We Regulate a Tiny Fraction of the 12,000 ‘Forever Chemicals.’ There’s a Better Way.

By Kathleen Blackburn

Dr. Blackburn teaches creative nonfiction writing at the University of Chicago.

When I was 12 years old, I sat inside a raucous tent revival in West Texas, gripping my seat in fear that a traveling evangelist would accuse me of killing my father.

A healthy former Air Force pilot who’d averaged an eight-minute mile in the New York City Marathon, my father had just been diagnosed with advanced colorectal cancer and been given a short time to live. Nothing about his predicament made sense to our family at the time. He was 38, a nonsmoker and nondrinker, with no history of cancer in his family.

My parents were conservative evangelicals deeply skeptical of the medical industry, and his diagnosis kicked their beliefs into high gear. When doctors couldn’t answer our questions — Why did Dad have cancer? What could we do? — we sought out faith healers who did. Traveling evangelists and local preachers claimed that the cancer was, in fact, a satanic attack. This gave us a way out: We simply had to muster enough faith to believe a miracle was possible and God would heal him.

What no one in my family knew at the time was that for most of his life my father had been exposed to perfluoroalkyl and polyfluoroalkyl substances, the synthetic compounds known collectively as PFAS, which have been linked to increased risk of certain cancers . His fallow muscle, jaundiced skin and weight loss were very likely because of the decades-long accumulation of carcinogenic chemicals in the drinking water at the military sites where he had lived and worked since his childhood.

The environmental violence exacted by PFAS, like the effects of radiation and polychlorinated biphenyls, or PCBs, can be difficult to prove. Only a few studies have examined the relationship between PFAS exposure and colorectal cancer (though the Yale School of Public Health has estimated that around 80 percent of cases are linked to environmental exposure). But on April 10 the Environmental Protection Agency announced the first federal mandate to limit the level of six PFAS in tap water. Going forward, water systems where they are detected will be required to remove them. Michael Regan, the E.P.A. administrator, called the announcement “life-changing,” and for me it was — it validated what I’d long suspected, that exposure to these chemicals can be devastating.

But if six PFAS sounds like a small number, that’s because it is. At this point, more than 12,000 formulations of PFAS exist and only a fifth of Americans’ PFAS exposure comes from drinking water. That means additional PFAS that have not been targeted for regulation persist in our water, soil and consumer products, leaving many Americans vulnerable to exposure. To reduce the risk they pose, we need far more comprehensive mandates that test, monitor and limit the entire class of PFAS chemicals.

In the 1930s and ’40s, manufacturing companies like DuPont and 3M began developing these substances for use as repellent in nonstick items including Teflon pans, Scotchgard and firefighting foams. But the chemical bonds that make them so useful as a repellent also make PFAS nearly indestructible; it’s why they have been labeled “forever chemicals.” They don’t break down once they enter the environment, and instead they accumulate in water, soil and our bodies.

Firefighting foams have been a major source of PFAS contamination since their development in the 1960s. In collaboration with the U.S. Navy, 3M produced foams that the Defense Department sprayed in routine fire drills and emergencies around the country. The chemicals eventually leached into groundwater at military sites like the ones where my father lived and water sources surrounding them. In 2000, 3M began phasing out its use of perfluorooctanyl sulfonate, a component of PFAS-containing firefighting foam, citing health concerns. Still, it was not until 2023 that the Department of Defense was banned from purchasing foams containing PFAS.

The E.P.A.’s move this month to regulate PFAS is a significant next step, but even in places where the groundwater is not highly contaminated, we will all still be exposed to unregulated PFAS without further government action. The chemicals are used in a staggering number of consumer products, including carpet, pizza boxes, microwave popcorn, yoga pants, bags and toiletries like dental floss, shampoo and cosmetics. They are still key ingredients in some firefighting foams; many fire departments still use these foams in emergencies like chemical plant fires. And in Texas, thousands of pounds of PFAS are being shot into the ground to lubricate drill bits for fracking.

We already know that high levels of exposure to PFAS have been linked to disastrous health impacts like birth defects, liver damage and many kinds of cancer. Yet the rate at which PFAS are being released into the environment far outpaces toxicologists’ ability to study their consequences for human health. Some 31 percent of groundwater samples in places with no known source of PFAS have shown contamination levels that exceed E.P.A. limits. And in some locations with established sources, like military and industrial sites, the levels of PFAS are far higher than the standard set by the new rule.

We now need a federal ban on firefighting foams containing PFAS and regulations that are enforceable by law to limit not just specific compounds in our water, but the whole class of highly pervasive chemicals. Mandates should identify the historical sources of pollution to hold industries accountable and avoid further straining the communities exposed to PFAS with the additional cost of their cleanup. On Friday, the E.P.A. helpfully put two PFAS compounds under its Superfund authority, shifting accountability for cleanup from taxpayers to polluters.

I am now 39, the age my father was when he died from cancer in 1998. Nearly 20 years passed before I discovered that the Defense Department is responsible for a significant portion of the PFAS pollution in the United States and that dangerously high levels of PFAS have been confirmed or are suspected of contaminating the drinking water at military sites from Guam to Universal City, Texas, including where my father had lived as a child and worked as an Air Force officer. My father was no longer an officer when he was diagnosed, but the reality of PFAS exposure shows that we carry the traces of each place we’ve lived even after we’ve left.

This month’s federal announcement cannot resurrect the dead. Still, it gives context to tragedies that made no sense at the time and sent my family into a desperate search for a miracle that never came.

I would never wish such a revelation on my 2-year-old son’s generation. I would not have them blindly searching for answers that first manifest, as so often quests through oblivion do, in blaming oneself. This is exactly what companies like 3M and DuPont hope will continue happening — that those of us who were first exposed will still bear the burden of proof.

We should not have to risk repeated exposure to these substances, with the most powerful bonds in organic chemistry, caused by the willful negligence of industry each time we place our faith in a glass of water. Let’s not wait for more long-term effects on our health before we act.

Kathleen Blackburn teaches creative nonfiction writing at the University of Chicago. She is the author of “Loose of Earth.”

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