Cancer prevention

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Cancer prevention is the practice of taking active measures to decrease the incidence of cancer and mortality. [1] [2] The practice of prevention depends on both individual efforts to improve lifestyle and seek preventive screening, and socioeconomic or public policy related to cancer prevention. [3] Globalized cancer prevention is regarded as a critical objective due to its applicability to large populations, reducing long term effects of cancer by promoting proactive health practices and behaviors, and its perceived cost-effectiveness and viability for all socioeconomic classes. [2]

Contents

The majority of cancer cases are due to the accumulation of environmental pollution being inherited as epigenetic damage and most of these environmental factors are controllable lifestyle choices. [4] Greater than a reported 75% of cancer deaths could be prevented by avoiding risk factors including: tobacco, overweight / obesity, an insufficient diet, physical inactivity, alcohol, sexually transmitted infections, and air pollution. [5] Not all environmental causes are controllable, such as naturally occurring background radiation, and other cases of cancer are caused through hereditary genetic disorders. Current genetic engineering techniques under development may serve as preventive measures in the future. [6] Future preventive screening measures can be additionally improved by minimizing invasiveness and increasing specificity by taking individual biological makeup into account, also known as "population-based personalized cancer screening." [2]

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Death rate adjusted for age for malignant cancer per 100,000 inhabitants in 2004.

While anyone can get cancer, [8] age is one of the biggest factors that increases the risk of cancer: 3 out of 4 cancers are found in people aged 55 or older.

Risk reduction

Dietary

Advertisement for a healthy diet to possibly reduce cancer risk Make healthy choices poster.jpg
Advertisement for a healthy diet to possibly reduce cancer risk

An average 35% of human cancer mortality is attributed to the diet of the individual. [9] Studies have linked excessive consumption of red or processed meat to an increased risk of breast cancer, colon cancer, and pancreatic cancer, a phenomenon which could be due to the presence of carcinogens in meats cooked at high temperatures. [10] [11]

Dietary recommendations for reducing cancer risk typically include an emphasis on vegetables, fruit, whole grains, and fish, and an avoidance of processed and red meat (beef, pork, lamb), animal fats, and refined carbohydrates. [12] [13] The World Cancer Research Fund recommends a diet rich in fruits and vegetables to reduce the risk of cancer. A diet rich in foods of plant origin, including non-starchy fruits and vegetables, non-starchy roots and tubers, and whole grains, may have protective effects against cancer. [14] Consumption of coffee is associated with a reduced risk of liver cancer. [15] Substituting processed foods, such as biscuits, cakes or white bread – which are high in fat, sugars and refined starches – with a plant-based diet may reduce the risk of cancer. [14]

While many dietary recommendations have been proposed to reduce the risk of cancer, the evidence to support them is not definitive. [12] [13] The primary dietary factors that increase risk are obesity and alcohol consumption; with a diet low in fruits and vegetables and high in red meat being implicated but not confirmed. [16] [17] A 2014 meta-analysis did not find a relationship between consuming fruits and vegetables and reduced cancer risk. [18]

Physical activity

Research shows that regular physical activity may help to reduce cancer up to 30%, [19] [20] [21] with up to 300 minutes per week of moderate to vigorous intensity of physical activity recommended. [22] [23] Even though, the beneficial effect of exercise relative to cancer development is known, there is a lack of clear understanding of the mechanisms underlying this relationship. [24] Some potential mechanisms by which physical activity minimises cancer risk are alterations in free radical generation, alterations in steroid hormones, changes in body composition, and direct effects on the tumour. Different biological pathways involved in cancer have been studied suggesting that physical activity reduces cancer risk by helping weight control, [23] reducing hormones such as estrogen and insulin, reducing inflammation, and strengthening the immune system. [21] [25] Steroid hormones have significant effects on the development of reproductive cancer, and exercise minimises cancer risks by regulating steroid hormones. [24] Similarly, exercise affects cancers that can be controlled by the immune system's ability through immune enhancement. [24]

Medication and supplements

In the general population, NSAIDs reduce the risk of colorectal cancer; however, due to the cardiovascular and gastrointestinal side effects, they cause overall harm when used to lower cancer risk. [26] Aspirin has been found to reduce the risk of death from cancer by about 7%. [27] COX-2 inhibitors may decrease the rate of polyp formation in people with familial adenomatous polyposis however are associated with the same adverse effects as NSAIDs. [28] Daily use of tamoxifen or raloxifene has been demonstrated to reduce the risk of developing breast cancer in high-risk women. [29] The benefit verses harm for 5-alpha-reductase inhibitor such as finasteride is not clear. [30]

Vitamins have not been found to be effective at reducing cancer risk, [31] although low blood levels of vitamin D are correlated with increased cancer risk. [32] [33] Whether this relationship is causal and vitamin D supplementation is protective is not determined. [34] Beta-carotene supplementation has been found to increase lung cancer rates in those who are at high risk. [35] Folic acid supplementation has not been found effective in preventing colon cancer and may increase colon polyps. [36] A 2018 systematic review concluded that selenium has no beneficial effect in reducing the risk of cancer based on high quality evidence. [37]

Avoidance of carcinogens

The United States National Toxicology Program (NTP) has identified the chemical substances listed below as known human carcinogens in the NTP's 15th Report on Carcinogens. Simply because a substance has been designated as a carcinogen, however, does not mean that the substance will necessarily cause cancer. Many factors influence whether a person exposed to a carcinogen will develop cancer, including the amount and duration of the exposure and the individual's genetic background. [38]

Ingestion

Inhalation

Skin exposure

Vaccination

Anti-cancer vaccines can be preventive or be used as therapeutic treatment. [2] All such vaccines incite adaptive immunity by enhancing cytotoxic T lymphocyte (CTL) recognition and activity against tumor-associated or tumor-specific antigens (TAA and TSAs).

Vaccines have been developed that prevent infection by some carcinogenic viruses. [39] Human papillomavirus vaccine (Gardasil and Cervarix) decreases the risk of developing cervical cancer. [39] The hepatitis B vaccine prevents infection with hepatitis B virus and thus decreases the risk of liver cancer. [39] The administration of human papillomavirus and hepatitis B vaccinations is recommended when resources allow. [40]

Some cancer vaccines are usually immunoglobulin-based and target antigens specific to cancer or abnormal human cells. [2] [41] These vaccines may be given to treat cancer during the progression of disease to boost the immune system's ability to recognize and attack cancer antigens as foreign entities. Antibodies for cancer cell vaccines may be taken from the patient's own body (autologous vaccine) or from another patient (allogeneic vaccine). [39] Several autologous vaccines, such as Oncophage for kidney cancer and Vitespen for a variety of cancers, have either been released or are undergoing clinical trial. FDA-approved vaccines, such as Sipuleucel-T for metastasizing prostate cancer or Nivolumab for melanoma and lung cancer can act either by targeting over-expressed or mutated proteins or by temporarily inhibiting immune checkpoints to boost immune activity. [2] [42]

Screening

Screening procedures, commonly sought for more prevalent cancers, such as colon, breast, and cervical, have greatly improved in the past few decades from advances in biomarker identification and detection. [2] Early detection of pancreatic cancer biomarkers was accomplished using a SERS-based immunoassay approach. [43] A SERS-based multiplex protein biomarker detection platform in a microfluidic chip can be used to detect several protein biomarkers to predict the type of disease and critical biomarkers and increase the chance of diagnosis between diseases with similar biomarkers (e.g. pancreatic cancer, ovarian cancer, and pancreatitis). [44]

To improve the chances of detecting cancer early, all eligible people should take advantage of cancer screening services. However, overall uptake of cancer screening among the general population is not widespread, especially among disadvantaged groups (e.g. those with low income, mental illnesses, or are from different ethnic groups) who face different barriers that lead to lower attendance rates. [45]

Cervical cancer

Cervical cancer is usually screened through in vitro examination of the cells of the cervix (e.g. Pap smear), colposcopy, or direct inspection of the cervix (after application of dilute acetic acid), or testing for HPV, the oncogenic virus that is the necessary cause of cervical cancer. [39] Screening is recommended for women over 21 years, initially women between 21 and 29 years old are encouraged to receive Pap smear screens every three years, and those over 29 every five years. [2] For women older than the age of 65 and with no history of cervical cancer or abnormality, and with an appropriate precedence of negative Pap test results may cease regular screening. [46]

Still, adherence to recommended screening plans depends on age and may be linked to "educational level, culture, psychosocial issues, and marital status," further emphasizing the importance of addressing these challenges in regards to cancer screening. [2]

Colorectal cancer

Colorectal cancer is most often screened with the fecal occult blood test (FOBT). Variants of this test include guaiac-based FOBT (gFOBT), the fecal immunochemical test (FIT), and stool DNA testing (sDNA). [47] Further testing includes flexible sigmoidoscopy (FS), total colonoscopy (TC), or computed tomography (CT) scans if a total colonoscopy is non-ideal. A recommended age at which to begin screening is 50 years. However, this is highly dependent on medical history and exposure to risk factors for colorectal cancer. Effective screening has been shown to reduce the incidence of colorectal cancer by 33% and colorectal cancer mortality by 43%. [2]

Breast cancer

The estimated number of new breast cancer cases in the US in 2018 is predicted to be more than 1.7 million, with more than six hundred thousand deaths. [48] Factors such as breast size, reduced physical activity, obesity and overweight status, infertility and never having had children, hormone replacement therapy (HRT), and genetics are risk factors for breast cancer. [2] Mammograms are widely used to screen for breast cancer, and are recommended for women 50–74 years of age by the US Preventive Services Task Force (USPSTF). However, the USPSTF does not recommend mammograms for women 40–49 years old due to the possibility of overdiagnosis. [2] [49]

Preventable causes of cancer

As of 2017, tobacco use, diet and nutrition, physical activity, obesity/overweight status, infectious agents, and chemical and physical carcinogens have been reported to be the leading areas where cancer prevention can be practiced through enacting positive lifestyle changes, getting appropriate regular screening, and getting vaccinated. [50]

The development of many common cancers are incited by such risk factors. For example, consumption of tobacco and alcohol, a medical history of genital warts and STDs, immunosuppression, unprotected sex, and early age of first sexual intercourse and pregnancy all may serve as risk factors for cervical cancer. Obesity, red meat or processed meat consumption, tobacco and alcohol, and a medical history of inflammatory bowel diseases are all risk factors for colorectal cancer (CRC). On the other hand, exercise and consumption of vegetables may help decrease the risk of CRC. [2]

Several preventable causes of cancer were highlighted in Doll and Peto's landmark 1981 study, [5] estimating that 75 – 80% of cancers in the United States could be prevented by avoidance of 11 different factors. A 2013 review of more recent cancer prevention literature by Schottenfeld et al., [51] summarizing studies reported between 2000 and 2010, points to most of the same avoidable factors identified by Doll and Peto. However, Schottenfeld et al. considered fewer factors (e.g. non inclusion of diet) in their review than Doll and Peto, and indicated that avoidance of these fewer factors would result in prevention of 60% of cancer deaths. The table below indicates the proportions of cancer deaths attributed to different factors, summarizing the observations of Doll and Peto, Shottenfeld et al. and several other authors, and shows the influence of major lifestyle factors on the prevention of cancer, such as tobacco, an unhealthy diet, obesity and infections.

Proportions of cancer deaths in the United States attributed to different factors
FactorDoll &
Peto [5] [ needs update ]		Schottenfeld
et al. [51] 		Other reports
Tobacco 30%30%38% men, 23% women, [52] 30%, [53] 25-30%
Unhealthy diet 35%-32%, [54] 10%, [55] 30-35%
Obesity *10%14% women, 20% men, among non-smokers, [56] 10-20%, 19-20% United States, 16-18% Great Britain, 13% Brazil, 11-12% China [57]
Infection†10%5-8%7-10%, [58] 8% developed nations, 26% developing nations, [53] 10% high income, 25% African
Alcohol 3%3-4%3.6%, [53] 8% USA, 20% France [59]
Occupational exposures4%3-5%2-10%, may be 15-20% in men [60]
Radiation (solar and ionizing) 3%3-4%up to 10%
Physical inactivity *<5%7% [61]
Reproductive and sexual behavior1-13%--
Pollution2%[ needs update ]--
Medicines and medical procedures1%--
Industrial products<1%[ needs update ]--
Food additives<1%[ needs update ]--

*Included in diet

†Carcinogenic infections include: for the uterine cervix (human papillomavirus [HPV]), liver (hepatitis B virus [HBV] and hepatitis C virus [HCV]), stomach ( Helicobacter pylori [H pylori]), lymphoid tissues (Epstein-Barr virus [EBV]), nasopharynx (EBV), urinary bladder ( Schistosoma hematobium ), and biliary tract ( Opisthorchis viverrini, Clonorchis sinensis )

History of cancer prevention

Cancer has been thought to be a preventable disease since the time of Roman physician Galen, who observed that an unhealthy diet was correlated with cancer incidence. In 1713, Italian physician Ramazzini hypothesized that abstinence caused lower rates of cervical cancer in nuns. Further observation in the 18th century led to the discovery that certain chemicals, such as tobacco, soot and tar (leading to scrotal cancer in chimney sweeps, as reported by Percivall Pott in 1775), could serve as carcinogens for humans. Although Pott suggested preventive measures for chimney sweeps (wearing clothes to prevent contact bodily contact with soot), his suggestions were only put into practice in Holland, resulting in decreasing rates of scrotal cancer in chimney sweeps. Later, the 19th century brought on the onset of the classification of chemical carcinogens. [62]

In the early 20th century, physical and biological carcinogens, such as X-ray radiation or the Rous Sarcoma Virus discovered 1911, were identified. Despite observed correlation of environmental or chemical factors with cancer development, there was a deficit of formal prevention research and lifestyle changes for cancer prevention were not feasible during this time. [62]

In Europe, in 1987 the European Commission launched the European Code Against Cancer to help educate the public about actions they can take to reduce their risk of getting cancer. [63] The first version of the code covered 10 recommendations covering tobacco, alcohol, diet, weight, sun exposure, exposure to known carcinogens, early detection and participation in organized breast and cervical cancer screening programs. [64] In the early 1990s, the European School of Oncology led a review of the code and added details about the scientific evidence behind each of the recommendations. [64] Later updates were coordinated by the International Agency for Research on Cancer. The fourth edition of the code, , developed in 2012‒2013, also includes recommendations on participation in vaccination programs for hepatitis B (infants) and human papillomavirus (girls), breast feeding and hormone replacement therapy, and participation in organized colorectal cancer screening programs.

See also

Related Research Articles

<span class="mw-page-title-main">Carcinogen</span> Substance, radionuclide, or radiation directly involved in causing cancer

A carcinogen is any agent that promotes the development of cancer. Carcinogens can include synthetic chemicals, naturally occurring substances, physical agents such as ionizing and non-ionizing radiation, and biologic agents such as viruses and bacteria. Most carcinogens act by creating mutations in DNA that disrupt a cell's normal processes for regulating growth, leading to uncontrolled cellular proliferation. This occurs when the cell's DNA repair processes fail to identify DNA damage allowing the defect to be passed down to daughter cells. The damage accumulates over time. This is typically a multi-step process during which the regulatory mechanisms within the cell are gradually dismantled allowing for unchecked cellular division.

<span class="mw-page-title-main">Cervical cancer</span> Cancer arising from the cervix

Cervical cancer is a cancer arising from the cervix or in any layer of the wall of the cervix. It is due to the abnormal growth of cells that have the ability to invade or spread to other parts of the body. Early on, typically no symptoms are seen. Later symptoms may include abnormal vaginal bleeding, pelvic pain or pain during sexual intercourse. While bleeding after sex may not be serious, it may also indicate the presence of cervical cancer.

<span class="mw-page-title-main">Breast cancer</span> Cancer that originates in mammary glands

Breast cancer is a cancer that develops from breast tissue. Signs of breast cancer may include a lump in the breast, a change in breast shape, dimpling of the skin, milk rejection, fluid coming from the nipple, a newly inverted nipple, or a red or scaly patch of skin. In those with distant spread of the disease, there may be bone pain, swollen lymph nodes, shortness of breath, or yellow skin.

<span class="mw-page-title-main">Cancer</span> Group of diseases involving cell growth

Cancer is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body. These contrast with benign tumors, which do not spread. Possible signs and symptoms include a lump, abnormal bleeding, prolonged cough, unexplained weight loss, and a change in bowel movements. While these symptoms may indicate cancer, they can also have other causes. Over 100 types of cancers affect humans.

<span class="mw-page-title-main">Human papillomavirus infection</span> Human disease

Human papillomavirus infection is caused by a DNA virus from the Papillomaviridae family. Many HPV infections cause no symptoms and 90% resolve spontaneously within two years. In some cases, an HPV infection persists and results in either warts or precancerous lesions. These lesions, depending on the site affected, increase the risk of cancer of the cervix, vulva, vagina, penis, anus, mouth, tonsils, or throat. Nearly all cervical cancer is due to HPV, and two strains – HPV16 and HPV18 – account for 70% of all cases. HPV16 is responsible for almost 90% of HPV-positive oropharyngeal cancers. Between 60% and 90% of the other cancers listed above are also linked to HPV. HPV6 and HPV11 are common causes of genital warts and laryngeal papillomatosis.

<span class="mw-page-title-main">Colorectal cancer</span> Cancer of the colon or rectum

Colorectal cancer (CRC), also known as bowel cancer, colon cancer, or rectal cancer, is the development of cancer from the colon or rectum. Signs and symptoms may include blood in the stool, a change in bowel movements, weight loss, abdominal pain and fatigue. Most colorectal cancers are due to lifestyle factors and genetic disorders. Risk factors include diet, obesity, smoking, and lack of physical activity. Dietary factors that increase the risk include red meat, processed meat, and alcohol. Another risk factor is inflammatory bowel disease, which includes Crohn's disease and ulcerative colitis. Some of the inherited genetic disorders that can cause colorectal cancer include familial adenomatous polyposis and hereditary non-polyposis colon cancer; however, these represent less than 5% of cases. It typically starts as a benign tumor, often in the form of a polyp, which over time becomes cancerous.

<span class="mw-page-title-main">Cardiovascular disease</span> Class of diseases that involve the heart or blood vessels

Cardiovascular disease (CVD) is any disease involving the heart or blood vessels. CVDs constitute a class of diseases that includes: coronary artery diseases, heart failure, hypertensive heart disease, rheumatic heart disease, cardiomyopathy, arrhythmia, congenital heart disease, valvular heart disease, carditis, aortic aneurysms, peripheral artery disease, thromboembolic disease, and venous thrombosis.

<span class="mw-page-title-main">Deoxycholic acid</span> Bile acid

Deoxycholic acid is a bile acid. Deoxycholic acid is one of the secondary bile acids, which are metabolic byproducts of intestinal bacteria. The two primary bile acids secreted by the liver are cholic acid and chenodeoxycholic acid. Bacteria metabolize chenodeoxycholic acid into the secondary bile acid lithocholic acid, and they metabolize cholic acid into deoxycholic acid. There are additional secondary bile acids, such as ursodeoxycholic acid. Deoxycholic acid is soluble in alcohol and acetic acid. When pure, it exists in a white to off-white crystalline powder form.

<span class="mw-page-title-main">Preventive healthcare</span> Prevention of the occurrence of diseases

Preventive healthcare, or prophylaxis, is the application of healthcare measures to prevent diseases. Disease and disability are affected by environmental factors, genetic predisposition, disease agents, and lifestyle choices, and are dynamic processes that begin before individuals realize they are affected. Disease prevention relies on anticipatory actions that can be categorized as primal, primary, secondary, and tertiary prevention.

<span class="mw-page-title-main">Women's Health Initiative</span> Long-term U.S. health study

The Women's Health Initiative (WHI) was a series of clinical studies initiated by the U.S. National Institutes of Health (NIH) in 1991, to address major health issues causing morbidity and mortality in postmenopausal women. It consisted of three clinical trials (CT) and an observational study (OS). In particular, randomized controlled trials were designed and funded that addressed cardiovascular disease, cancer, and osteoporosis.

Malignant transformation is the process by which cells acquire the properties of cancer. This may occur as a primary process in normal tissue, or secondarily as malignant degeneration of a previously existing benign tumor.

<span class="mw-page-title-main">Red meat</span> Meat which is red when raw, with high myoglobin content

In gastronomy, red meat is commonly red when raw, in contrast to white meat, which is pale in color before cooking. In culinary terms, only flesh from mammals or fowl is classified as red or white. In nutritional science, red meat is defined as any meat that has more of the protein myoglobin than white meat. White meat is defined as non-dark meat from fish or chicken.

<span class="mw-page-title-main">Alcohol and cancer</span> Relationship between cancer and the consumption of alcohol

Alcohol and cancer have a complex relationship. Alcohol causes cancers of the oesophagus, liver, breast, colon, oral cavity, rectum, pharynx, and larynx, and probably causes cancers of the pancreas. Cancer risk can occur even with light to moderate drinking. The more alcohol is consumed, the higher the cancer risk, and no amount can be considered completely safe.

<span class="mw-page-title-main">Diet and cancer</span> Connections between dietary habits and cancer

Many dietary recommendations have been proposed to reduce the risk of cancer, few have significant supporting scientific evidence. Obesity and drinking alcohol have been correlated with the incidence and progression of some cancers. Lowering the consumption of sweetened beverages is recommended as a measure to address obesity.

<span class="mw-page-title-main">Risk factors for breast cancer</span> Overview article

Risk factors for breast cancer may be divided into preventable and non-preventable. Their study belongs in the field of epidemiology. Breast cancer, like other forms of cancer, can result from multiple environmental and hereditary risk factors. The term environmental, as used by cancer researchers, means any risk factor that is not genetically inherited.

<span class="mw-page-title-main">Cancer screening</span> Method to detect cancer

The objective of cancer screening is to detect cancer before symptoms appear, involving various methods such as blood tests, urine tests, DNA tests, and medical imaging. The purpose of screening is early cancer detection, to make the cancer easier to treat and extending life expectancy. In 2019, cancer was the second leading cause of death globally; more recent data is pending due to the COVID-19 pandemic.

Cancer is caused by genetic changes leading to uncontrolled cell growth and tumor formation. The basic cause of sporadic (non-familial) cancers is DNA damage and genomic instability. A minority of cancers are due to inherited genetic mutations. Most cancers are related to environmental, lifestyle, or behavioral exposures. Cancer is generally not contagious in humans, though it can be caused by oncoviruses and cancer bacteria. The term "environmental", as used by cancer researchers, refers to everything outside the body that interacts with humans. The environment is not limited to the biophysical environment, but also includes lifestyle and behavioral factors.

The association between obesity, as defined by a body mass index of 30 or higher, and risk of a variety of types of cancer has received a considerable amount of attention in recent years. Obesity has been associated with an increased risk of esophageal cancer, pancreatic cancer, colorectal cancer, breast cancer, endometrial cancer, kidney cancer, thyroid cancer, liver cancer and gallbladder cancer. Obesity may also lead to increased cancer-related mortality. Obesity has also been described as the fat tissue disease version of cancer, where common features between the two diseases were suggested for the first time.

<span class="mw-page-title-main">Gynecologic cancer disparities in the United States</span>

Gynecologic cancer disparities in the United States refer to differences in incidence, prevalence, and mortality from gynecologic cancers between population groups. The five main types of gynecologic cancer include cervical cancer, ovarian cancer, endometrial cancer, vaginal cancer, and vulvar cancer. For patients with these and other gynecologic malignancies within the United States, disparities across the care continuum by socioeconomic status and racial/ethnic background have been previously identified and studied. The causes behind these disparities are multifaceted and a complex interplay of systemic differences in health as well as individual patient factors such as cultural, educational, and economic barriers.

Marian L. Neuhouser is an American epidemiologist who is the Head of Cancer Prevention at the Fred Hutchinson Cancer Center. Her research focuses on the role of nutrition in the prevention of cancer.

References

  1. ↑ "Cancer prevention: 7 steps to reduce your risk". Mayo Clinic. September 27, 2008. Retrieved January 30, 2010.[ unreliable medical source? ]
  2. 1 2 3 4 5 6 7 8 9 10 11 12 13 Valle I, Tramalloni D, Bragazzi NL (June 2015). "Cancer prevention: state of the art and future prospects". Journal of Preventive Medicine and Hygiene. 56 (1): E21–7. PMC   4718348 . PMID   26789828.
  3. ↑ "Cancer Prevention & Early Detection Facts & Figures 2017-18" (PDF). Cancer.org. April 1, 2017.
  4. ↑ Danaei G, Vander Hoorn S, Lopez AD, et al. (2005). "Causes of cancer in the world: comparative risk assessment of nine behavioural and environmental risk factors". Lancet. 366 (9499): 1784–93. doi: 10.1016/S0140-6736(05)67725-2 . PMID   16298215. S2CID   17354479.
  5. 1 2 3 Doll R, Peto R (1981). "The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today". J. Natl. Cancer Inst. 66 (6): 1191–308. doi:10.1093/jnci/66.6.1192. PMID   7017215.
  6. ↑ "CRISPR Gene-Editing Tool May Help Improve Cancer Immunotherapy". National Cancer Institute. March 20, 2017. Retrieved March 9, 2018.
  7. ↑ "WHO Disease and injury country estimates". World Health Organization. 2009. Retrieved November 11, 2009.
  8. ↑ "Cancer Prevention". February 12, 2014. Archived from the original on June 17, 2018. Retrieved November 7, 2014.
  9. ↑ Surh YJ (2003). "Cancer chemoprevention with dietary phytochemicals". Nature Reviews Cancer. 3 (10): 768–780. doi:10.1038/nrc1189. PMID   14570043.
  10. ↑ Zheng W, Lee SA (2009). "Well-done meat intake, heterocyclic amine exposure, and cancer risk". Nutr Cancer. 61 (4): 437–46. doi:10.1080/01635580802710741. PMC   2769029 . PMID   19838915.
  11. ↑ Ferguson LR (February 2010). "Meat and cancer". Meat Sci. 84 (2): 308–13. doi:10.1016/j.meatsci.2009.06.032. PMID   20374790.
  12. 1 2 Kushi LH, Doyle C, McCullough M, et al. (2012). "American Cancer Society Guidelines on nutrition and physical activity for cancer prevention: reducing the risk of cancer with healthy food choices and physical activity". CA Cancer J Clin. 62 (1): 30–67. doi: 10.3322/caac.20140 . PMID   22237782.
  13. 1 2 Wicki A, Hagmann J (September 2011). "Diet and cancer". Swiss Medical Weekly . 141: w13250. doi: 10.4414/smw.2011.13250 . PMID   21904992.
  14. 1 2 "Eat wholegrains, vegetables, fruit and beans". World Cancer Research Fund International. 2023. Retrieved September 2, 2024.
  15. ↑ Larsson SC, Wolk A (May 2007). "Coffee consumption and risk of liver cancer: a meta-analysis". Gastroenterology. 132 (5): 1740–5. doi: 10.1053/j.gastro.2007.03.044 . PMID   17484871.
  16. ↑ Cappellani A, Di Vita M, Zanghi A, et al. (2012). "Diet, obesity and breast cancer: an update". Front Biosci. 4 (1): 90–108. doi:10.2741/253. PMID   22202045.
  17. ↑ Key TJ (January 2011). "Fruit and vegetables and cancer risk". Br. J. Cancer. 104 (1): 6–11. doi:10.1038/sj.bjc.6606032. PMC   3039795 . PMID   21119663.
  18. ↑ Wang X, Ouyang Y, Liu J, et al. (July 2014). "Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer: systematic review and dose-response meta-analysis of prospective cohort studies". BMJ. 349: g4490. doi:10.1136/bmj.g4490. PMC   4115152 . PMID   25073782.
  19. ↑ Moore SC, Lee IM, Weiderpass E, et al. (June 2016). "Association of Leisure-Time Physical Activity With Risk of 26 Types of Cancer in 1.44 Million Adults". JAMA Internal Medicine. 176 (6): 816–25. doi:10.1001/jamainternmed.2016.1548. PMC   5812009 . PMID   27183032.
  20. ↑ Kruk J, Czerniak U (2013). "Physical activity and its relation to cancer risk: updating the evidence". Asian Pacific Journal of Cancer Prevention. 14 (7): 3993–4003. doi: 10.7314/APJCP.2013.14.7.3993 . PMID   23991944.
  21. 1 2 "Physical Activity and Cancer". US National Cancer Institute. February 10, 2020. Retrieved January 12, 2025.
  22. ↑ Rock CL, Thomson C, Gansler T, et al. (2020). "American Cancer Society guideline for diet and physical activity for cancer prevention". CA: A Cancer Journal for Clinicians. 70 (4): 245–271. doi: 10.3322/caac.21591 . ISSN   0007-9235. PMID   32515498.
  23. 1 2 Friedenreich CM, Ryder-Burbidge C, McNeil J (2021). "Physical activity, obesity and sedentary behavior in cancer etiology: epidemiologic evidence and biologic mechanisms". Molecular Oncology. 15 (3): 790–800. doi:10.1002/1878-0261.12772. ISSN   1574-7891. PMC   7931121 . PMID   32741068.
  24. 1 2 3 Westerlind KC (2003). "Physical Activity and Cancer Prevention???Mechanisms:". Medicine & Science in Sports & Exercise. 35 (11): 1834–1840. doi:10.1249/01.MSS.0000093619.37805.B7. ISSN   0195-9131.
  25. ↑ Winzer BM, Whiteman DC, Reeves MM, et al. (June 2011). "Physical activity and cancer prevention: a systematic review of clinical trials". Cancer Causes & Control. 22 (6): 811–26. doi:10.1007/s10552-011-9761-4. PMID   21461921. S2CID   8687281.
  26. ↑ Rostom A, Dubé C, Lewin G, et al. (March 2007). "Nonsteroidal anti-inflammatory drugs and cyclooxygenase-2 inhibitors for primary prevention of colorectal cancer: a systematic review prepared for the U.S. Preventive Services Task Force". Annals of Internal Medicine. 146 (5): 376–389. doi:10.7326/0003-4819-146-5-200703060-00010. PMID   17339623. S2CID   23290390.
  27. ↑ Rothwell PM, Fowkes FG, Belch JF, et al. (January 2011). "Effect of daily aspirin on long-term risk of death due to cancer: analysis of individual patient data from randomised trials". Lancet. 377 (9759): 31–41. doi:10.1016/S0140-6736(10)62110-1. PMID   21144578. S2CID   22950940.
  28. ↑ Cooper K, Squires H, Carroll C, et al. (June 2010). "Chemoprevention of colorectal cancer: systematic review and economic evaluation". Health Technol Assess. 14 (32): 1–206. doi: 10.3310/hta14320 . PMID   20594533.
  29. ↑ Thomsen A, Kolesar JM (December 2008). "Chemoprevention of breast cancer". Am J Health Syst Pharm. 65 (23): 2221–2228. doi:10.2146/ajhp070663. PMID   19020189.
  30. ↑ Wilt TJ, MacDonald R, Hagerty K, et al. (2008). Wilt TJ (ed.). "Five-alpha-reductase Inhibitors for prostate cancer prevention". Cochrane Database Syst Rev (2): CD007091. doi:10.1002/14651858.CD007091. PMC   11270836 . PMID   18425978.
  31. ↑ "Vitamins and minerals: not for cancer or cardiovascular prevention". Prescrire Int. 19 (108): 182. August 2010. PMID   20939459.
  32. ↑ Giovannucci E, Liu Y, Rimm EB, et al. (April 2006). "Prospective study of predictors of vitamin D status and cancer incidence and mortality in men". J. Natl. Cancer Inst. 98 (7): 451–459. CiteSeerX   10.1.1.594.1654 . doi:10.1093/jnci/djj101. PMID   16595781.
  33. ↑ "Vitamin D Has Role in Colon Cancer Prevention". Archived from the original on December 4, 2006. Retrieved July 27, 2007.
  34. ↑ Schwartz GG, Blot WJ (April 2006). "Vitamin D status and cancer incidence and mortality: something new under the sun". J. Natl. Cancer Inst. 98 (7): 428–30. doi: 10.1093/jnci/djj127 . PMID   16595770.
  35. ↑ Fritz H, Kennedy D, Fergusson D, et al. (2011). Minna JD (ed.). "Vitamin A and retinoid derivatives for lung cancer: a systematic review and meta analysis". PLOS ONE. 6 (6): e21107. Bibcode:2011PLoSO...621107F. doi: 10.1371/journal.pone.0021107 . PMC   3124481 . PMID   21738614.
  36. ↑ Cole BF, Baron JA, Sandler RS, et al. (June 2007). "Folic acid for the prevention of colorectal adenomas: a randomized clinical trial". JAMA. 297 (21): 2351–2359. doi:10.1001/jama.297.21.2351. PMID   17551129.
  37. ↑ Vinceti M, Filippini T, Del Giovane C, et al. (January 2018). "Selenium for preventing cancer". The Cochrane Database of Systematic Reviews. 1 (1): CD005195. doi:10.1002/14651858.CD005195.pub4. ISSN   1469-493X. PMC   6491296 . PMID   29376219.
  38. ↑ "Cancer-Causing Substances in the Environment". NCI. National Cancer Institute of the United States. June 17, 2022. Retrieved June 4, 2024.PD-icon.svg This article incorporates text from this source, which is in the public domain .
  39. 1 2 3 4 5 "Cancer Vaccine Fact Sheet". NCI. June 8, 2006. Archived from the original on October 25, 2008. Retrieved November 15, 2008.
  40. ↑ Lertkhachonsuk AA, Yip CH, Khuhaprema T, et al. (2013). "Cancer prevention in Asia: resource-stratified guidelines from the Asian Oncology Summit 2013". Lancet Oncology. 14 (12): e497–507. doi:10.1016/S1470-2045(13)70350-4. PMID   24176569.
  41. ↑ "What's new in cancer immunotherapy research?". www.cancer.org. Retrieved March 9, 2018.
  42. ↑ Pardoll DM (March 2012). "The blockade of immune checkpoints in cancer immunotherapy". Nature Reviews. Cancer. 12 (4): 252–264. doi:10.1038/nrc3239. PMC   4856023 . PMID   22437870.
  43. ↑ Banaei N, et al. (September 2017). "Multiplex detection of pancreatic cancer biomarkers using a SERS-based immunoassay". Nanotechnology. 28 (45): 455101. Bibcode:2017Nanot..28S5101B. doi:10.1088/1361-6528/aa8e8c. PMID   28937361. S2CID   206086640.
  44. ↑ Banaei N, et al. (January 2019). "Machine learning algorithms enhance the specificity of cancer biomarker detection using SERS-based immunoassays in microfluidic chips". RSC Advances. 9 (4): 1859–1868. Bibcode:2019RSCAd...9.1859B. doi: 10.1039/c8ra08930b . PMC   9059745 . PMID   35516124.
  45. ↑ "Catching cancer early: how research could help us improve". NIHR Evidence (Plain English summary). November 10, 2021. doi:10.3310/collection_48071. S2CID   244006179.
  46. ↑ "Ages 65 Years and Older: Exams and Screening Tests - ACOG". www.acog.org. Retrieved April 21, 2018.
  47. ↑ Janz T, Lu K, Povlow MR, et al. (December 2016). "A Review of Colorectal Cancer Detection Modalities, Stool DNA, and Fecal Immunochemistry Testing in Adults Over the Age of 50". Cureus. 8 (12): e931. doi: 10.7759/cureus.931 . PMC   5235652 . PMID   28097082.
  48. ↑ "Cancer Facts & Figures 2018" (PDF).
  49. ↑ "Final Update Summary: Breast Cancer: Screening - US Preventive Services Task Force". www.uspreventiveservicestaskforce.org. Archived from the original on March 10, 2018. Retrieved April 21, 2018.
  50. ↑ "Cancer Prevention & Early Detection Facts & Figures 2017-18" (PDF). Cancer.org. April 1, 2017.
  51. 1 2 Schottenfeld D, Beebe-Dimmer JL, Buffler PA, et al. (2013). "Current perspective on the global and United States cancer burden attributable to lifestyle and environmental risk factors". Annu Rev Public Health. 34: 97–117. doi:10.1146/annurev-publhealth-031912-114350. PMID   23514316.
  52. ↑ Shopland DR (1995). "Tobacco use and its contribution to early cancer mortality with a special emphasis on cigarette smoking". Environ. Health Perspect. 103 (Suppl 8): 131–42. Bibcode:1995EnvHP.103S.131S. doi:10.1289/ehp.95103s8131. PMC   1518977 . PMID   8741773.
  53. 1 2 3 Parsa N (2012). "Environmental factors inducing human cancers". Iran. J. Public Health. 41 (11): 1–9. PMC   3521879 . PMID   23304670.
  54. ↑ Willett WC (1995). "Diet, nutrition, and avoidable cancer". Environ. Health Perspect. 103 (Suppl 8): 165–70. Bibcode:1995EnvHP.103S.165W. doi:10.1289/ehp.95103s8165. PMC   1518978 . PMID   8741778.
  55. ↑ Trichopoulou A, Lagiou P, Kuper H, et al. (2000). "Cancer and Mediterranean dietary traditions". Cancer Epidemiol. Biomarkers Prev. 9 (9): 869–73. PMID   11008902.
  56. ↑ Song M, Giovannucci E (2016). "Estimating the Influence of Obesity on Cancer Risk: Stratification by Smoking Is Critical". J. Clin. Oncol. 34 (27): 3237–9. doi:10.1200/JCO.2016.67.6916. PMID   27458311.
  57. ↑ "2.7.1 Body fatness and foods and drinks that promote weight gain". Policy and Action for Cancer Prevention. Food, Nutrition, and Physical Activity: a Global Perspective. Washington DC, USA: World Cancer Research Fund/American Institute for Cancer Research. 2009. p. 22. ISBN   978-0-9722522-4-9.
  58. ↑ Schottenfeld D, Beebe-Dimmer J (2006). "Chronic inflammation: a common and important factor in the pathogenesis of neoplasia". CA Cancer J Clin. 56 (2): 69–83. doi: 10.3322/canjclin.56.2.69 . PMID   16514135.
  59. ↑ Tuyns AJ (1979). "Epidemiology of alcohol and cancer". Cancer Res. 39 (7 Pt 2): 2840–3. PMID   445490.
  60. ↑ Irigaray P, Newby JA, Clapp R, et al. (2007). "Lifestyle-related factors and environmental agents causing cancer: an overview". Biomed. Pharmacother. 61 (10): 640–58. doi:10.1016/j.biopha.2007.10.006. PMID   18055160.
  61. ↑ Moore SC, Lee IM, Weiderpass E, et al. (2016). "Association of Leisure-Time Physical Activity With Risk of 26 Types of Cancer in 1.44 Million Adults". JAMA Intern Med. 176 (6): 816–25. doi:10.1001/jamainternmed.2016.1548. PMC   5812009 . PMID   27183032.
  62. 1 2 Bode AM, Dong Z (July 2009). "Cancer prevention research - then and now". Nature Reviews. Cancer. 9 (7): 508–16. doi:10.1038/nrc2646. PMC   2838238 . PMID   19536108.
  63. ↑ Unspecified (May 8, 1990). Europe against cancer programme: Report on the implementation of the first plan of action, 1987-1989 (PDF) (Report). Communication from the European Commission to the Council, the European Parliament and the Economic and Social Committee. COM (90) 185 final. Via Archive of European Integration (AEI)
  64. 1 2 Boyle, Peter, et al. (September 1995). "European School of Oncology Advisory Report to the European Commission for the "Europe Against Cancer Programme", European Code Against Cancer". Eur J Cancer. 31 (9): 1395‒1403. doi:10.1016/0959-8049(95)00334-F. PMID   7577062.
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