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Cancer prevention

From Wikipedia, the free encyclopedia

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]

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]

Death rate adjusted for age for malignant cancer per 100,000 inhabitants in 2004.[7]

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

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Dietary

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Main article: Diet and cancer
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] More specifically, a higher risk of breast cancer also has been shown to possibly be associated with a higher intake of red and processed meats, refined sugars, alcohol and saturated fats.[12] Researchers suggest that this association may be due to the inflammation processes and the increase of estrogen and testosterone from the foods in this diet.[12] In some cases, a high intake of eggs was also found to may be associated with a higher risk of breast cancer due to its high cholesterol contents.[12]

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.[13][14] 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.[15] Consumption of coffee is associated with a reduced risk of liver cancer and endometrial cancer.[16][17] Additionally, a higher coffee intake was shown to be related to a lower risk of melanoma and oral/pharyngeal cancer.[17] However, a higher risk of childhood acute lymphocytic leukemia and bladder cancer actually is associated with higher coffee intake.[17] However, it's important to note that these claims are associations and there is not strong evidence that validates the effects of coffee consumption and cancer risk.[17] 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.[15] In some cases, plant-based diets have shown to be inversely associated with overall cancer risk.[18]

While many dietary recommendations have been proposed to reduce the risk of cancer, the evidence to support them is not definitive.[13][14] 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.[19][20] A 2014 meta-analysis did not find a relationship between consuming fruits and vegetables and reduced cancer risk.[21]

Green Tea

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Green tea comes from camellia sinensis and is made in a process that does not use fermentation.[22] Some studies have found that green tea could possibly have positive effects relating to cancer prevention.[22] Research shows that over half the studies (58%) they examined found that drinking green tea may prevent certain cancers, such as esophageal, stomach, pancreatic, liver and colorectal cancer.[22] But due to the various methodological problems that come with this type of research, the review concludes that the overall analysis of green tea consumption and cancer prevention is inconclusive.[22]

Physical activity

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Research shows that regular physical activity may help to reduce cancer up to 30%,[23][24][25] with up to 300 minutes per week of moderate to vigorous intensity of physical activity recommended.[26][27]

Possible mechanisms by which physical activity may reduce cancer risk include lowering levels of estrogen and insulin, reducing inflammation, and strengthening the immune system.[25][28]

Medication and supplements

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In the general population, NSAIDs reduce the risk of colorectal cancer [29]; however, due to the cardiovascular and gastrointestinal side effects, they cause overall harm when used to lower cancer risk.[30] Aspirin use after a cancer diagnosis is associated with about a 20% reduction in cancer mortality.[31] 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.[32] Daily use of tamoxifen or raloxifene has been demonstrated to reduce the risk of developing breast cancer in high-risk women.[33] The benefit verses harm for 5-alpha-reductase inhibitor such as finasteride is not clear.[34]

Vitamins supplements have not been found to be effective at reducing overall cancer risk,[35] although observational studies consistently show that low blood levels of vitamin D are correlated with increased cancer risk.[36][37] Whether this relationship is causal and vitamin D supplementation is protective is not determined.[38] Beta-carotene supplementation has been found to increase lung cancer rates in those who are at high risk.[39] Folic acid supplementation has not been found effective in preventing colon cancer and may increase colon polyps.[40] A 2018 systematic review concluded that selenium has no beneficial effect in reducing the risk of cancer based on high quality evidence.[41]

Avoidance of carcinogens

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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.[42]

Ingestion

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Inhalation

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Skin exposure

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Recent Updates in Carcinogen Classification

Updated evaluations by the International Agency for Research on Cancer (IARC) continue to confirm the carcinogenicity of long-recognized agents such as asbestos and benzene, which are included above in the NTP 15th report on carcinogens, while also guiding the assessment of emerging substances in consumer products. A meta-analysis published in 2023 found that exposure to certain endocrine-disrupting chemicals, including p,p′-DDT (and its metabolite p,p′-DDE) and several polychlorinated biphenyl (PCB) variants, was associated with increased risk of breast cancer.[43]

Genetic and Epigenetic Factors in Cancer Prevention

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Genetic factors play a significant role in cancer risk, adding to the influence of modifiable environmental factors. Specific gene polymorphisms are associated with increased cancer risk. For instance, variations in the vitamin D receptor (VDR) gene are associated with elevated risks of both breast and ovarian cancers, suggesting that impaired vitamin D signaling may contribute to carcinogenesis.[44][45] Similarly, inherited variations in the enzymes that contribute to the metabolism of carcinogens have been linked with an increased risk of colorectal cancer, demonstrating how genetic differences can affect the capacity of the body to break down cancer-causing substances.[46] In addition to these inherited factors, environmental exposures can also alter gene regulation through epigenetic modifications. A systematic review on epigenetics, microbiota, and breast cancer revealed that factors like maternal diet and stress may alter epigenetic markers and impact the development and progression of breast cancer.[47] Research on gene-environment interactions in colorectal cancer identified that lifestyle factors – such as the intake of processed meats, alcohol consumption, and the use of aspirin – affect cancer risk in individuals of specific genetic backgrounds, with aspirin’s protective effects varying according to genetic makeup.[48]

Vaccination

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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.[49] Human papillomavirus vaccine (Gardasil and Cervarix) decreases the risk of developing cervical cancer.[49] The hepatitis B vaccine prevents infection with hepatitis B virus and thus decreases the risk of liver cancer.[49] The administration of human papillomavirus and hepatitis B vaccinations is recommended when resources allow.[50]

Some cancer vaccines are usually immunoglobulin-based and target antigens specific to cancer or abnormal human cells.[2][51] 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).[49] 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][52]

Screening

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Main article: Cancer 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.[53] 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).[54]

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.[55] Research indicates that these screening barriers are influenced by both individual circumstances and area-level factors. A systematic review of lung cancer screenings found that feelings of fear, anxiety, and negative attitudes toward the screening process can discourage individuals from participating.[56] Additionally, a review examining clinical and psychosocial aspects associated with breast, cervical, and colorectal cancer screening found that factors like personal beliefs, social support, and effective communication with healthcare providers are associated with screening attendance.[57]

Beyond the personal and psychosocial factors, broader socioeconomic elements also impact screening participation rates. Women with lower income are 20% more likely to not participate in breast cancer screening, with lower education increasing the likelihood of skipping screening by 18%. Immigrant women have nearly triple the odds of non-participation, and individuals living further away from their assigned screening facility, as well as those with a male family doctor, are also less likely to participate in screening.[58] Rural communities often face significant transportation barriers, with long travel distances and limited access to public transportation further reducing access to screening services. In addition, in these rural areas, the uneven distribution of healthcare providers and limited availability of telehealth services can exacerbate these disparities, reducing access to specialized cancer screening.[59]

The Role of Health Literacy in Cancer Prevention

Health literacy – the ability to navigate and use health care information – is an important factor in cancer prevention. Studies show that individuals with better health literacy are more likely to follow through with cancer screening programs for breast, cervical, and colorectal cancers.[60] Some intervention programs aimed at improving health literacy are shown to not only boost understanding of health information but also address psychosocial aspects, such as patient communication and decision conflict.[61] These interventions include patient decision aids, multimedia educational tools, and clinician communication training, which are linked to improvements in patient knowledge, risk perception, and comfortability with screening processes. Enhancing health literacy by addressing patients' informational and emotional needs may help to reduce disparities in cancer prevention.

Cervical cancer

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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.[49] 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.[62]

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

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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).[63] Further testing includes flexible sigmoidoscopy (FS), total colonoscopy (TC), or computed tomography (CT) scans if a total colonoscopy is non-ideal. The recommended age at which to begin and continue screening is 50–75 years.[2][64] However, this is highly dependent on medical history and exposure to risk factors for colorectal cancer.[2] Effective screening has been shown to reduce the incidence of colorectal cancer by 33% and colorectal cancer mortality by 43%.[2]

Breast cancer

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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.[65] 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][66]

Breast Cancer Prevention

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Breast cancer is a leading cause of death for women worldwide, being the most common diagnosis for females in regards to cancer.[67] Current research outlines the possible ability for physical activity and diet to help breast cancer prevention.

Physical Activity

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Researchers have found a link between physical activity and a reduced risk, recurrence and mortality in relation to breast cancer.[67] Physical activity has been shown to plays a crucial role in helping the immune system against cancer.[68] Physical activity and body mass index (BMI) are interrelated because of how an increase of physical activity possibly may decrease BMI, which has also shown to be a breast cancer prevention factor.[67] A recent meta-analysis examined 45,000 breast cancer patients and concluded that women who had higher levels of physical activity showed a possible lower risk for breast cancer recurrence and an overall lower risk of mortality from breast cancer.[69] Additionally, mammary tumor growth or volume was also shown to have possibly reduced due to physical activity.[67] When looking at metastasis, two studies found that physical activity may have reduced the metastasis of breast cancer that was present in the lungs, femur or abdominal area.[67] In one meta-analysis it was shown that for every 25 hours/week of nonoccupational activity breast cancer risk may be reduced by up to 2%, for every 10 hours/week of exercise breast cancer risk can be possibly be reduced by 3%, and for every 2 hours/week of moderate-to-vigorous recreational activity can possibly reduce breast cancer risk by 5%.[68] In some cases, physical activity has also been shown to lower the level of sex hormones, which in turn can possibly decrease breast cancer risk among women.[68]

The Mediterranean Diet (MedDiet)

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With the rise of new research, it's been suggested that the MedDiet may lower the risk of breast cancer.[68] Some research shows that following this diet could help with breast cancer risk, particularly among women who are postmenopausal.[70] However, other studies have not found an association between the MedDiet and breast cancer risk.[71] The MedDiet is known to be a healthy diet because it focuses on eating foods that are plant-based and high in carbohydrates and antioxidants, which has been shown to help reduce inflammation.[68] This diet includes foods such as various whole grains, nuts, beans, vegetables, fruits, herbs, spices, and olive oil as well as focusing on eating lean sources of meat such as fish and poultry instead of processed proteins.[68][71]

In some studies, there has been an inverse association between breast cancer risk and whole grain consumption.[68][72] Research suggests certain aspects as to why whole grains can possibly help prevent breast cancer. Various bioactive phytochemicals including phenolic acids, alkylresorcinols, lignans, vitamin E, polysaccharides, carotenoids, phytosterols, and anthocyanins are present in whole grains.[68] These components are said to help prevent breast carcinogenesis.[68] However, other studies done have shown no association between breast cancer risk and whole grain intake.[72] Another food group, legumes, has been shown to possible lower breast cancer risk due to its high fiber contents.[68] An example of this food group that would be encouraged to eat is lentils, peas, beans and chickpeas.[68] One study found that women who ate >5.5 servings of fruit and vegetables per day had a 11% lower chance of getting breast cancer, compared to those who ate <2.5 servings per day.[68] Researchers suggested this was due to the antioxidants and micronutrients that have been shown to help reduce breast cancer risk.[68] However, other research shows that there is no association between pre- and postmenopausal breast cancer and eating foods with carotenoids or non-starchy vegetables.[71]

Preventable causes of cancer

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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.[73]

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 more recent review of Doll and Peto's work confirmed that most of these estimates remain relevant today.[74] In addition, a 2013 review of more recent cancer prevention literature by Schottenfeld et al.,[75] 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
Factor Doll &
Peto[5][needs update]		 Schottenfeld
et al.[75]		 Other reports
Tobacco 30% 30% 38% men, 23% women,[76] 30%,[77] 25-30%
Unhealthy diet 32% - 20%,[78] 10%,[79] 10%-20%
Obesity * 10% 14% women, 20% men, among non-smokers,[80] 10-20%, 19-20% United States, 16-18% Great Britain, 13% Brazil, 11-12% China[81]
Infection† 10% 5-8% 7-10%,[82] 8% developed nations, 26% developing nations,[77] 10% high income, 25% African
Alcohol 3% 3-4% 3.6%,[77] 8% USA, 20% France[83]
Occupational exposures 4% 3-5% 2-10%, may be 15-20% in men[84]
Radiation (solar and ionizing) 3% 3-4% up to 10%
Physical inactivity * <5% 7%[23]
Reproductive and sexual behavior 1-13% - -
Pollution 2%[needs update] - -
Medicines and medical procedures 1% - -
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

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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.[85]

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.[85]

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.[86] 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.[87] 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.[87] Later updates were coordinated by the International Agency for Research on Cancer. The fourth edition of the code, [1], 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

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References

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  1. ^ "Cancer prevention: 7 steps to reduce your risk". Mayo Clinic. September 27, 2008. Retrieved January 30, 2010.[unreliable medical source?]
  2. ^ a b c d e f g h i j k l m n o 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 – E27. 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, Murray CJ, Ezzati M (November 2005). "Causes of cancer in the world: comparative risk assessment of nine behavioural and environmental risk factors". Lancet. 366 (9499): 1784–1793. doi:10.1016/S0140-6736(05)67725-2. PMID 16298215. S2CID 17354479.
  5. ^ a b c Doll R, Peto R (June 1981). "The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today". Journal of the National Cancer Institute. 66 (6): 1191–1308. 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 (October 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". Nutrition and Cancer. 61 (4): 437–446. doi:10.1080/01635580802710741. PMC 2769029. PMID 19838915.
  11. ^ Ferguson LR (February 2010). "Meat and cancer". Meat Science. 84 (2): 308–313. doi:10.1016/j.meatsci.2009.06.032. PMID 20374790.
  12. ^ a b c Buja A, Pierbon M, Lago L, Grotto G, Baldo V (July 2020). "Breast Cancer Primary Prevention and Diet: An Umbrella Review". International Journal of Environmental Research and Public Health. 17 (13): 4731. doi:10.3390/ijerph17134731. PMC 7369836. PMID 32630215.
  13. ^ a b Kushi LH, Doyle C, McCullough M, Rock CL, Demark-Wahnefried W, Bandera EV, 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. 62 (1): 30–67. doi:10.3322/caac.20140. PMID 22237782.
  14. ^ a b Wicki A, Hagmann J (September 2011). "Diet and cancer". Swiss Medical Weekly. 141: w13250. doi:10.4414/smw.2011.13250. PMID 21904992.
  15. ^ a b "Eat wholegrains, vegetables, fruit and beans". World Cancer Research Fund International. 2023. Retrieved September 2, 2024.
  16. ^ Yu C, Cao Q, Chen P, Yang S, Deng M, Wang Y, et al. (December 2, 2016). "An updated dose–response meta-analysis of coffee consumption and liver cancer risk". Scientific Reports. 6 (1): 37488. Bibcode:2016NatSR...637488Y. doi:10.1038/srep37488. ISSN 2045-2322. PMC 5133591. PMID 27910873.
  17. ^ a b c d Zhao LG, Li ZY, Feng GS, Ji XW, Tan YT, Li HL, et al. (December 2020). "Coffee drinking and cancer risk: an umbrella review of meta-analyses of observational studies". BMC Cancer. 20 (1): 101. doi:10.1186/s12885-020-6561-9. ISSN 1471-2407. PMC 7003434. PMID 32024485.
  18. ^ DeClercq V, Nearing JT, Sweeney E (June 2022). "Plant-Based Diets and Cancer Risk: What is the Evidence?". Current Nutrition Reports. 11 (2): 354–369. doi:10.1007/s13668-022-00409-0. ISSN 2161-3311. PMID 35334103.
  19. ^ Cappellani A, Di Vita M, Zanghi A, Cavallaro A, Piccolo G, Veroux M, et al. (January 2012). "Diet, obesity and breast cancer: an update". Frontiers in Bioscience. 4 (1): 90–108. doi:10.2741/253. PMID 22202045.
  20. ^ Key TJ (January 2011). "Fruit and vegetables and cancer risk". British Journal of Cancer. 104 (1): 6–11. doi:10.1038/sj.bjc.6606032. PMC 3039795. PMID 21119663.
  21. ^ Wang X, Ouyang Y, Liu J, Zhu M, Zhao G, Bao W, 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.
  22. ^ a b c d Liu J, Xing J, Fei Y (2008). "Green tea (Camellia sinensis) and cancer prevention: a systematic review of randomized trials and epidemiological studies". Chinese Medicine. 3 (1): 12. doi:10.1186/1749-8546-3-12. ISSN 1749-8546. PMC 2577676. PMID 18940008.
  23. ^ a b Moore SC, Lee IM, Weiderpass E, Campbell PT, Sampson JN, Kitahara CM, 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): 816–825. doi:10.1001/jamainternmed.2016.1548. PMC 5812009. PMID 27183032.
  24. ^ 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.
  25. ^ a b "Physical Activity and Cancer". US National Cancer Institute. February 10, 2020. Retrieved January 12, 2025.
  26. ^ Rock CL, Thomson C, Gansler T, Gapstur SM, McCullough ML, Patel AV, et al. (July 2020). "American Cancer Society guideline for diet and physical activity for cancer prevention". CA. 70 (4): 245–271. doi:10.3322/caac.21591. PMID 32515498.
  27. ^ Friedenreich CM, Ryder-Burbidge C, McNeil J (March 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. PMC 7931121. PMID 32741068.
  28. ^ Winzer BM, Whiteman DC, Reeves MM, Paratz JD (June 2011). "Physical activity and cancer prevention: a systematic review of clinical trials". Cancer Causes & Control. 22 (6): 811–826. doi:10.1007/s10552-011-9761-4. PMID 21461921. S2CID 8687281.
  29. ^ Bosetti C, Santucci C, Gallus S, Martinetti M, La Vecchia C (May 2020). "Aspirin and the risk of colorectal and other digestive tract cancers: an updated meta-analysis through 2019". Annals of Oncology. 31 (5): 558–568. doi:10.1016/j.annonc.2020.02.012. hdl:2434/730600.
  30. ^ Guirguis-Blake JM, Evans CV, Perdue LA, Bean SI, Senger CA (April 26, 2022). "Aspirin Use to Prevent Cardiovascular Disease and Colorectal Cancer: Updated Evidence Report and Systematic Review for the US Preventive Services Task Force". JAMA. 327 (16): 1585. doi:10.1001/jama.2022.3337. ISSN 0098-7484.
  31. ^ Elwood PC, Morgan G, Delon C, Protty M, Galante J, Pickering J, et al. (July 2, 2021). "Aspirin and cancer survival: a systematic review and meta-analyses of 118 observational studies of aspirin and 18 cancers". ecancermedicalscience. 15. doi:10.3332/ecancer.2021.1258. PMC 8426031. PMID 34567243.
  32. ^ Cooper K, Squires H, Carroll C, Papaioannou D, Booth A, Logan RF, et al. (June 2010). "Chemoprevention of colorectal cancer: systematic review and economic evaluation". Health Technology Assessment. 14 (32): 1–206. doi:10.3310/hta14320. PMID 20594533.
  33. ^ Manna ED, Serrano D, Aurilio G, Bonanni B, Lazzeroni M (August 21, 2023). "Chemoprevention and Lifestyle Modifications for Risk Reduction in Sporadic and Hereditary Breast Cancer". Healthcare. 11 (16): 2360. doi:10.3390/healthcare11162360. ISSN 2227-9032. PMC 10454363. PMID 37628558.
  34. ^ Wilt TJ, MacDonald R, Hagerty K, Schellhammer P, Kramer BS (April 2008). Wilt TJ (ed.). "Five-alpha-reductase Inhibitors for prostate cancer prevention". The Cochrane Database of Systematic Reviews. 2008 (2): CD007091. doi:10.1002/14651858.CD007091. PMC 11270836. PMID 18425978.
  35. ^ "Vitamins and minerals: not for cancer or cardiovascular prevention". Prescrire International. 19 (108): 182. August 2010. PMID 20939459.
  36. ^ Kim H, Giovannucci E (2020), Reichrath J (ed.), "Vitamin D Status and Cancer Incidence, Survival, and Mortality", Sunlight, Vitamin D and Skin Cancer, vol. 1268, Cham: Springer International Publishing, pp. 39–52, doi:10.1007/978-3-030-46227-7_3, ISBN 978-3-030-46226-0, PMID 32918213, retrieved April 13, 2025
  37. ^ "Vitamin D Has Role in Colon Cancer Prevention". Archived from the original on December 4, 2006. Retrieved July 27, 2007.
  38. ^ Schwartz GG, Blot WJ (April 2006). "Vitamin D status and cancer incidence and mortality: something new under the sun". Journal of the National Cancer Institute. 98 (7): 428–430. doi:10.1093/jnci/djj127. PMID 16595770.
  39. ^ Fritz H, Kennedy D, Fergusson D, Fernandes R, Doucette S, Cooley K, 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.
  40. ^ Cole BF, Baron JA, Sandler RS, Haile RW, Ahnen DJ, Bresalier 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.
  41. ^ Vinceti M, Filippini T, Del Giovane C, Dennert G, Zwahlen M, Brinkman M, et al. (January 2018). "Selenium for preventing cancer". The Cochrane Database of Systematic Reviews. 1 (1): CD005195. doi:10.1002/14651858.CD005195.pub4. PMC 6491296. PMID 29376219.
  42. ^ "Cancer-Causing Substances in the Environment". NCI. National Cancer Institute of the United States. June 17, 2022. Retrieved June 4, 2024. Public Domain This article incorporates text from this source, which is in the public domain.
  43. ^ Liu H, Sun Y, Ran L, Li J, Shi Y, Mu C, et al. (November 9, 2023). "Endocrine-disrupting chemicals and breast cancer: a meta-analysis". Frontiers in Oncology. 13. doi:10.3389/fonc.2023.1282651. ISSN 2234-943X. PMC 10665889. PMID 38023188.
  44. ^ Zhang K, Song L (April 25, 2014). Toland AE (ed.). "Association between Vitamin D Receptor Gene Polymorphisms and Breast Cancer Risk: A Meta-Analysis of 39 Studies". PLOS ONE. 9 (4): e96125. Bibcode:2014PLoSO...996125Z. doi:10.1371/journal.pone.0096125. ISSN 1932-6203. PMC 4000223. PMID 24769568.
  45. ^ Liu Y, Li C, Chen P, Li X, Li M, Guo H, et al. (June 24, 2013). Miao XP (ed.). "Polymorphisms in the Vitamin D Receptor (VDR) and the Risk of Ovarian Cancer: A Meta-Analysis". PLOS ONE. 8 (6): e66716. Bibcode:2013PLoSO...866716L. doi:10.1371/journal.pone.0066716. ISSN 1932-6203. PMC 3691226. PMID 23826116.
  46. ^ Sharzehan MA, Sito H, Abdullah N, Alexiou A, Papadakis M, Jamal R, et al. (November 23, 2022). "Association between CYP2E1 polymorphisms and colorectal cancer risk: a systematic review and meta-analysis". Scientific Reports. 12 (1): 20149. Bibcode:2022NatSR..1220149S. doi:10.1038/s41598-022-24398-w. ISSN 2045-2322. PMC 9684517. PMID 36418904.
  47. ^ Soldado-Gordillo A, Álvarez-Mercado AI (May 30, 2024). "Epigenetics, Microbiota, and Breast Cancer: A Systematic Review". Life. 14 (6): 705. Bibcode:2024Life...14..705S. doi:10.3390/life14060705. ISSN 2075-1729. PMC 11204553. PMID 38929688.
  48. ^ Yang T, Li X, Montazeri Z, Little J, Farrington SM, Ioannidis JP, et al. (November 2019). "Gene–environment interactions and colorectal cancer risk: An umbrella review of systematic reviews and meta-analyses of observational studies". International Journal of Cancer. 145 (9): 2315–2329. doi:10.1002/ijc.32057. ISSN 0020-7136. PMC 6767750. PMID 30536881.
  49. ^ a b c d e "Cancer Vaccine Fact Sheet". NCI. June 8, 2006. Archived from the original on October 25, 2008. Retrieved November 15, 2008.
  50. ^ Lertkhachonsuk AA, Yip CH, Khuhaprema T, Chen DS, Plummer M, Jee SH, et al. (November 2013). "Cancer prevention in Asia: resource-stratified guidelines from the Asian Oncology Summit 2013". The Lancet. Oncology. 14 (12): e497 – e507. doi:10.1016/S1470-2045(13)70350-4. PMID 24176569.
  51. ^ "What's new in cancer immunotherapy research?". www.cancer.org. Retrieved March 9, 2018.
  52. ^ 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.
  53. ^ Banaei N, Foley A, Houghton JM, Sun Y, Kim B (November 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.
  54. ^ Banaei N, Moshfegh J, Mohseni-Kabir A, Houghton JM, Sun Y, Kim B (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.
  55. ^ "Catching cancer early: how research could help us improve". NIHR Evidence (Plain English summary). November 10, 2021. doi:10.3310/collection_48071. S2CID 244006179.
  56. ^ McFadden K, Nickel B, Rankin NM, Li T, Jennett CJ, Sharman A, et al. (August 2024). "Participant factors associated with psychosocial impacts of lung cancer screening: A systematic review". Cancer Medicine. 13 (15). doi:10.1002/cam4.70054. ISSN 2045-7634. PMC 11297455. PMID 39096118.
  57. ^ Lemmo D, Martino ML, Vallone F, Donizzetti AR, Freda MF, Palumbo F, et al. (April 2023). "Clinical and psychosocial constructs for breast, cervical, and colorectal cancer screening participation: A systematic review". International Journal of Clinical and Health Psychology. 23 (2): 100354. doi:10.1016/j.ijchp.2022.100354. PMC 9677078. PMID 36415605.
  58. ^ Ding L, Wang J, Greuter M, Goossens M, van Hal G, de Bock G (October 2020). "Determinants of non-participation in population-based breast cancer screening: a systematic review and meta-analysis". European Journal of Cancer. 138: S2. doi:10.1016/S0959-8049(20)30535-9.
  59. ^ Wercholuk AN, Parikh AA, Snyder RA (September 2022). "The Road Less Traveled: Transportation Barriers to Cancer Care Delivery in the Rural Patient Population". JCO Oncology Practice. 18 (9): 652–662. doi:10.1200/OP.22.00122. ISSN 2688-1527.
  60. ^ Baccolini V, Isonne C, Salerno C, Giffi M, Migliara G, Mazzalai E, et al. (February 2022). "The association between adherence to cancer screening programs and health literacy: A systematic review and meta-analysis". Preventive Medicine. 155: 106927. doi:10.1016/j.ypmed.2021.106927. hdl:11573/1616880.
  61. ^ Housten AJ, Gunn CM, Paasche-Orlow MK, Basen-Engquist KM (April 2021). "Health Literacy Interventions in Cancer: a Systematic Review". Journal of Cancer Education. 36 (2): 240–252. doi:10.1007/s13187-020-01915-x. ISSN 0885-8195. PMC 8005416. PMID 33155097.
  62. ^ "Ages 65 Years and Older: Exams and Screening Tests - ACOG". www.acog.org. Retrieved April 21, 2018.
  63. ^ Janz T, Lu K, Povlow MR, Urso B (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.
  64. ^ Fitzpatrick-Lewis D, Ali MU, Warren R, Kenny M, Sherifali D, Raina P (December 2016). "Screening for Colorectal Cancer: A Systematic Review and Meta-Analysis". Clinical Colorectal Cancer. 15 (4): 298–313. doi:10.1016/j.clcc.2016.03.003. PMID 27133893.
  65. ^ "Cancer Facts & Figures 2018" (PDF).
  66. ^ "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.
  67. ^ a b c d e Xu Y, Rogers CJ (October 8, 2020). "Physical Activity and Breast Cancer Prevention: Possible Role of Immune Mediators". Frontiers in Nutrition. 7. doi:10.3389/fnut.2020.557997. ISSN 2296-861X. PMC 7578403. PMID 33134306.
  68. ^ a b c d e f g h i j k l m Dilnaz F, Zafar F, Afroze T, Zakia UB, Chowdhury T, Swarna SS, et al. (August 19, 2021). "Mediterranean Diet and Physical Activity: Two Imperative Components in Breast Cancer Prevention". Cureus. 13 (8): e17306. doi:10.7759/cureus.17306. ISSN 2168-8184. PMC 8451519. PMID 34567862.
  69. ^ Cormie P, Zopf EM, Zhang X, Schmitz KH (January 1, 2017). "The Impact of Exercise on Cancer Mortality, Recurrence, and Treatment-Related Adverse Effects". Epidemiologic Reviews. 39 (1): 71–92. doi:10.1093/epirev/mxx007. ISSN 0193-936X. PMID 28453622.
  70. ^ González-Palacios Torres C, Barrios-Rodríguez R, Muñoz-Bravo C, Toledo E, Dierssen T, Jiménez-Moleón JJ (April 2023). "Mediterranean diet and risk of breast cancer: An umbrella review". Clinical Nutrition. 42 (4): 600–608. doi:10.1016/j.clnu.2023.02.012. hdl:10481/81628. PMID 36893621.
  71. ^ a b c González-Palacios Torres C, Barrios-Rodríguez R, Muñoz-Bravo C, Toledo E, Dierssen T, Jiménez-Moleón JJ (April 2023). "Mediterranean diet and risk of breast cancer: An umbrella review". Clinical Nutrition. 42 (4): 600–608. doi:10.1016/j.clnu.2023.02.012. hdl:10481/81628. PMID 36893621.
  72. ^ a b Xiao Y, Ke Y, Wu S, Huang S, Li S, Lv Z, et al. (September 2018). "Association between whole grain intake and breast cancer risk: a systematic review and meta-analysis of observational studies". Nutrition Journal. 17 (1): 87. doi:10.1186/s12937-018-0394-2. ISSN 1475-2891. PMC 6201708. PMID 30241536.
  73. ^ "Cancer Prevention & Early Detection Facts & Figures 2017-18" (PDF). Cancer.org. April 1, 2017.
  74. ^ Blot WJ, Tarone RE (March 3, 2015). "Doll and Peto's Quantitative Estimates of Cancer Risks: Holding Generally True for 35 Years". JNCI Journal of the National Cancer Institute. 107 (4): djv044. doi:10.1093/jnci/djv044. ISSN 0027-8874. PMID 25739419.
  75. ^ a b Schottenfeld D, Beebe-Dimmer JL, Buffler PA, Omenn GS (2013). "Current perspective on the global and United States cancer burden attributable to lifestyle and environmental risk factors". Annual Review of Public Health. 34: 97–117. doi:10.1146/annurev-publhealth-031912-114350. PMID 23514316.
  76. ^ Shopland DR (November 1995). "Tobacco use and its contribution to early cancer mortality with a special emphasis on cigarette smoking". Environmental Health Perspectives. 103 (Suppl 8): 131–142. Bibcode:1995EnvHP.103S.131S. doi:10.1289/ehp.95103s8131. PMC 1518977. PMID 8741773.
  77. ^ a b c Parsa N (2012). "Environmental factors inducing human cancers". Iranian Journal of Public Health. 41 (11): 1–9. PMC 3521879. PMID 23304670.
  78. ^ Blot WJ, Tarone RE (March 3, 2015). "Doll and Peto's Quantitative Estimates of Cancer Risks: Holding Generally True for 35 Years". JNCI Journal of the National Cancer Institute. 107 (4): djv044 – djv044. doi:10.1093/jnci/djv044. ISSN 0027-8874.
  79. ^ Trichopoulou A, Lagiou P, Kuper H, Trichopoulos D (September 2000). "Cancer and Mediterranean dietary traditions". Cancer Epidemiology, Biomarkers & Prevention. 9 (9): 869–873. PMID 11008902.
  80. ^ Song M, Giovannucci E (September 2016). "Estimating the Influence of Obesity on Cancer Risk: Stratification by Smoking Is Critical". Journal of Clinical Oncology. 34 (27): 3237–3239. doi:10.1200/JCO.2016.67.6916. PMID 27458311.
  81. ^ "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.
  82. ^ Schottenfeld D, Beebe-Dimmer J (2006). "Chronic inflammation: a common and important factor in the pathogenesis of neoplasia". CA. 56 (2): 69–83. doi:10.3322/canjclin.56.2.69. PMID 16514135.
  83. ^ Tuyns AJ (July 1979). "Epidemiology of alcohol and cancer". Cancer Research. 39 (7 Pt 2): 2840–2843. PMID 445490.
  84. ^ Irigaray P, Newby JA, Clapp R, Hardell L, Howard V, Montagnier L, et al. (December 2007). "Lifestyle-related factors and environmental agents causing cancer: an overview". Biomedicine & Pharmacotherapy. 61 (10): 640–658. doi:10.1016/j.biopha.2007.10.006. PMID 18055160.
  85. ^ a b Bode AM, Dong Z (July 2009). "Cancer prevention research - then and now". Nature Reviews. Cancer. 9 (7): 508–516. doi:10.1038/nrc2646. PMC 2838238. PMID 19536108.
  86. ^ 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)
  87. ^ a b Boyle P, Veronesi U, Tubiana M, Alexander FE, da Silva F, Denis LJ, et al. (September 1995). "European School of Oncology Advisory report to the European Commission for the "Europe Against Cancer Programme" European Code Against Cancer". European Journal of Cancer. 31A (9): 1395–1405. doi:10.1016/0959-8049(95)00334-F. PMID 7577062.
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