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The causes of prostate cancer are poorly understood and there are no proven prevention measures.[1][2] Researchers continue to examine possible risk factors and preventive approaches.



Non-modifiable risk factors

Age

Increasing age is by far the most important risk factor for prostate cancer, with more than 80% of cases diagnosed in 2016 occurring in men 60 years of age or older.[3] Younger men diagnosed with prostate cancer are more likely to die prematurely from the disease than older men, as there is, on average, more of their lifetime left in which the cancer can progress and they are less likely to die of other causes.

Genetics

Family history of prostate cancer is a risk factor for the disease. Between five and 10% of prostate cancers may be due to an inherited genetic predisposition.[4][5] Men with first-degree relatives diagnosed with prostate cancer are two to three times more likely to develop prostate cancer compared to men with no affected relatives, and the risk may be higher if a first-degree relative was diagnosed before the age of 60 years.[6][7][8]

The genetic basis for familial prostate cancer is not fully understood. Men carrying mutations of the breast cancer susceptibility genes BRCA1 or BRCA2 have an increased risk of several types of cancer, including prostate cancer.[9] Male carriers of BRCA2 mutations have a 3.5-fold increased risk of prostate cancer[10] and an earlier age of onset[11] and have been reported to have poorer survival rates than those without BRCA2 mutations.[12][13][14]

A mutation of the gene HOXB13 has also been shown in recent research to substantially increase prostate cancer risk.[15]

Ethnicity

Analysis of NSW cancer registry data found that prostate cancer mortality 5-years after diagnosis was higher for Aboriginal men than non-Aboriginal men.[16] Even after adjusting for differences in demographic factors, stage at diagnosis, health access and comorbidities, Aboriginal men were 49% more likely to die from prostate cancer.[16]



Modifiable risk factors

Evidence on the links between prostate cancer risk and modifiable lifestyle factors is limited, with no conclusive evidence of an association identified by IARC.[17] A comprehensive review of the impact of diet and physical activity on cancer by the World Cancer Research Fund in 2018 concluded that there is strong evidence that overweight/obesity is associated with increased risk of prostate cancer.[18] While the association between higher pre-diagnosis body mass and higher risk of prostate cancer death is inconclusive,[19] evidence suggests there is poorer treatment outcomes among overweight and obese men with prostate cancer.

There was limited suggestive evidence that dairy products, diets high in calcium, low plasma alpha-tocopherol concentrations (vitamin E) and low plasma selenium concentrations increase the risk of prostate cancer.[18] This evidence falls below the threshold to make recommendations about dietary intake or supplement use.

Chemoprevention

Chemoprevention, or the use of natural or synthetic agents to reduce the incidence of cancer in those at increased risk, is being investigated but is not routinely used for prostate cancer.

The anti-androgen drug finasteride is thought to prevent prostate cancer, but this apparent benefit was limited to less aggressive cancers and it appeared that risk of more aggressive cancers was increased by the drug.[20][21] Dutasteride showed a decrease in prostate cancer incidence but unlike finasteride, an increase in aggressive cancers was not observed.[22] The United States Food and Drug Administration accepted the December 2010 advice of its Oncologic Drugs Advisory Committee that finasteride and dutasteride “do not have a favourable risk-benefit profile for the proposed use of chemoprevention of prostate cancer in healthy men”.[23]

A trial examining selenium and vitamin E supplementation in healthy men (The SELECT trial) found that these agents did not prevent prostate cancer[24] and that supplementation with vitamin E was associated with a significantly increased risk of prostate cancer of 17%.[25]


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References

  1.  Trottier G, Lawrentschuk N, Fleshner NE. Prevention strategies in prostate cancer. Curr Oncol 2010 Sep;17 Suppl 2:S4-10 Available from: http://www.ncbi.nlm.nih.gov/pubmed/20882132.
  2. Barry MJ, Simmons LH. Prevention of Prostate Cancer Morbidity and Mortality: Primary Prevention and Early Detection. Med Clin North Am 2017 Jul;101(4):787-806 Available from: http://www.ncbi.nlm.nih.gov/pubmed/28577627.
  3. Australian Institute of Health and Welfare. Cancer data in Australia. [homepage on the internet] Australian Institute of Health and Welfare; 2020 [cited 2021]. Available from: https://www.aihw.gov.au/reports/cancer/cancer-data-in-australia/contents/summary.
  4. Giri VN, Beebe-Dimmer JL. Familial prostate cancer. Semin Oncol 2016 Oct;43(5):560-565 Available from: http://www.ncbi.nlm.nih.gov/pubmed/27899188.
  5. Stanford JL, Ostrander EA. Familial Prostate Cancer. Epidemiologic Reviews 2001 [cited 2021];23(1):19-23 Available from: https://academic.oup.com/epirev/article/23/1/19/434786?searchresult=1.
  6. Bratt O. What should a urologist know about hereditary predisposition to prostate cancer? BJU Int 2007 Apr;99(4):743-7; discussion 747-8 Available from: http://www.ncbi.nlm.nih.gov/pubmed/17166238.
  7. Johns LE, Houlston RS. A systematic review and meta-analysis of familial prostate cancer risk. BJU Int 2003 Jun;91(9):789-94 Available from: http://www.ncbi.nlm.nih.gov/pubmed/12780833.
  8. Melia J, Hewitson P, Austoker J. Introduction: Review of screening for prostate cancer. BJU Int 2005 Apr;95 Suppl 3:1-3 Available from: http://www.ncbi.nlm.nih.gov/pubmed/15762868.
  9. Liede A, Metcalfe K, Hanna D, Hoodfar E, Snyder C, Durham C, et al. Evaluation of the needs of male carriers of mutations in BRCA1 or BRCA2 who have undergone genetic counseling. Am J Hum Genet 2000 Dec;67(6):1494-504 Available from: http://www.ncbi.nlm.nih.gov/pubmed/11063672.
  10. kConFab Investigators, Willems AJ, Dawson SJ, Samaratunga H, De Luca A, Antill YC, et al. Loss of heterozygosity at the BRCA2 locus detected by multiplex ligation-dependent probe amplification is common in prostate cancers from men with a germline BRCA2 mutation. Clin Cancer Res 2008 May 15;14(10):2953-61 Available from: http://www.ncbi.nlm.nih.gov/pubmed/18445692.
  11. Agalliu I, Karlins E, Kwon EM, Iwasaki LM, Diamond A, Ostrander EA, et al. Rare germline mutations in the BRCA2 gene are associated with early-onset prostate cancer. Br J Cancer 2007 Sep 17;97(6):826-31 Available from: http://www.ncbi.nlm.nih.gov/pubmed/17700570.
  12. Dobson R. Prostate cancer patients with BRCA2 mutation face poor survival. BMJ 2008 Jul 10;337:a705 Available from: http://www.ncbi.nlm.nih.gov/pubmed/18617489.
  13. Hereditary Breast Cancer Study Group, Narod SA, Neuhausen S, Vichodez G, Armel S, Lynch HT, et al. Rapid progression of prostate cancer in men with a BRCA2 mutation. Br J Cancer 2008 Jul 22;99(2):371-4 Available from: http://www.ncbi.nlm.nih.gov/pubmed/18577985.
  14. Tryggvadóttir L, Vidarsdóttir L, Thorgeirsson T, Jonasson JG, Olafsdóttir EJ, Olafsdóttir GH, et al. Prostate cancer progression and survival in BRCA2 mutation carriers. J Natl Cancer Inst 2007 Jun 20;99(12):929-35 Available from: http://www.ncbi.nlm.nih.gov/pubmed/17565157.
  15. Ewing CM, Ray AM, Lange EM, Zuhlke KA, Robbins CM, Tembe WD, et al. Germline mutations in HOXB13 and prostate-cancer risk. N Engl J Med 2012 Jan 12;366(2):141-9 Available from: http://www.ncbi.nlm.nih.gov/pubmed/22236224.
  16. Rodger JC, Supramaniam R, Gibberd AJ, Smith DP, Armstrong BK, Dillon A, et al. Prostate cancer mortality outcomes and patterns of primary treatment for Aboriginal men in New South Wales, Australia. BJU Int 2015 Apr;115 Suppl 5:16-23 Available from: http://www.ncbi.nlm.nih.gov/pubmed/25124107.
  17. International Agency for Research on Cancer. List of Classifications by cancer sites with sufficient or limited evidence in humans, IARC Monographs Volumes 1 to 129. [homepage on the internet] Lyon, France: IARC; 2020 [cited 2021 May 15]. Available from: https://monographs.iarc.who.int/wp-content/uploads/2019/07/Classifications_by_cancer_site.pdf.
  18. World Cancer Research Fund International. Diet, Nutrition, Physical Activity and Cancer: a Global Perspective - The Third Expert Report. [homepage on the internet] London, UK: World Cancer Research Fund International; 2018 Available from: https://www.wcrf.org/dietandcancer.
  19. Zhong J, Cao S, Gong W, Fei F, Wang M. Electronic Cigarettes Use and Intention to Cigarette Smoking among Never-Smoking Adolescents and Young Adults: A Meta-Analysis. Int J Environ Res Public Health 2016 May 3;13(5) Available from: http://www.ncbi.nlm.nih.gov/pubmed/27153077.
  20. Lebdai S, Bigot P, Azzouzi AR. High-grade prostate cancer and finasteride. BJU Int 2010 Feb;105(4):456-9 Available from: http://www.ncbi.nlm.nih.gov/pubmed/19930174.
  21. Thompson IM, Goodman PJ, Tangen CM, Lucia MS, Miller GJ, Ford LG, et al. The influence of finasteride on the development of prostate cancer. N Engl J Med 2003 Jul 17;349(3):215-24 Available from: http://www.ncbi.nlm.nih.gov/pubmed/12824459.
  22. REDUCE Study Group, Andriole GL, Bostwick DG, Brawley OW, Gomella LG, Marberger M, et al. Effect of dutasteride on the risk of prostate cancer. N Engl J Med 2010 Apr 1;362(13):1192-202 Available from: http://www.ncbi.nlm.nih.gov/pubmed/20357281.
  23. Theoret MR, Ning YM, Zhang JJ, Justice R, Keegan P, Pazdur R. The risks and benefits of 5α-reductase inhibitors for prostate-cancer prevention. N Engl J Med 2011;365(2):97-9 Available from: http://www.ncbi.nlm.nih.gov/pubmed/21675880.
  24. Lippman SM, Klein EA, Goodman PJ, Lucia MS, Thompson IM, Ford LG, et al. Effect of selenium and vitamin E on risk of prostate cancer and other cancers: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA 2009 Jan 7;301(1):39-51 Available from: http://www.ncbi.nlm.nih.gov/pubmed/19066370.
  25. Klein EA, Thompson IM Jr, Tangen CM, Crowley JJ, Lucia MS, Goodman PJ, et al. Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA 2011 Oct 12;306(14):1549-56 Available from: http://www.ncbi.nlm.nih.gov/pubmed/21990298.