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==Risk Factors==
==Risk Factors==
Common risk factors in the development of prostate cancer include:
Common risk factors in the development of prostate cancer include:
* '''Dietary'''
:* A diet high in fat, especially animal fat
:* A diet low in vegetables, fruits, and legumes
:* Food low or deficient in [[selenium]]
* '''Lifestyle'''
:* Men who abuse [[alcohol]]
* '''Family history'''
:* Men who have a father or brother with prostate cancer
* '''Occupation'''
:* Farmers
:* Tire plant workers
:* Painters
* '''Environmental factors'''
:* Men exposed to Agent Orange
:* Men who have been exposed to [[cadmium]]
* '''Medication'''
:* [[Fluoxymesterone]]


Note: A common problem in almost all men as they grow older is an enlarged prostate ([[benign prostatic hyperplasia]], or [[BPH]]). This problem does not raise the risk of prostate cancer.
===Genetic===
Genetic background may contribute to prostate cancer risk, as suggested by associations with race, family, and specific [[gene]] variants. Men who have a first-degree relative (father or brother) with prostate cancer have twice the risk of developing prostate cancer, and those with two first-degree relatives affected have a fivefold greater risk compared with men with no family history.<ref name="pmid2251225">{{cite journal | author = Steinberg GD, Carter BS, Beaty TH, Childs B, Walsh PC | title = Family history and the risk of prostate cancer | journal = Prostate | volume = 17 | issue = 4 | pages = 337–47 | year = 1990 | pmid = 2251225 | doi = 10.1002/pros.2990170409 }}</ref> In the United States, prostate cancer more commonly affects black men than white or Hispanic men, and is also more deadly in black men.<ref name="pmid9805030">{{cite journal | author = Gallagher RP, Fleshner N | title = Prostate cancer: 3. Individual risk factors | journal = CMAJ | volume = 159 | issue = 7 | pages = 807–13 | date = October 1998 | pmid = 9805030 | pmc = 1232741 | doi =  | url = http://www.cmaj.ca/cgi/reprint/159/7/807.pdf }}</ref><ref name="pmid11238701">{{cite journal | author = Hoffman RM, Gilliland FD, Eley JW, Harlan LC, Stephenson RA, Stanford JL, Albertson PC, Hamilton AS, Hunt WC, Potosky AL | title = Racial and ethnic differences in advanced-stage prostate cancer: the Prostate Cancer Outcomes Study | journal = J. Natl. Cancer Inst. | volume = 93 | issue = 5 | pages = 388–95 | date = March 2001 | pmid = 11238701 | doi = 10.1093/jnci/93.5.388 }}</ref> In contrast, the incidence and mortality rates for Hispanic men are one third lower than for non-Hispanic whites. [[Twin study|Studies of twins]] in [[Scandinavia]] suggest that 40% of prostate cancer risk can be explained by [[heritability|inherited factors]].<ref name="pmid10891514">{{cite journal | author = Lichtenstein P, Holm NV, Verkasalo PK, Iliadou A, Kaprio J, Koskenvuo M, Pukkala E, Skytthe A, Hemminki K | title = Environmental and heritable factors in the causation of cancer--analyses of cohorts of twins from Sweden, Denmark, and Finland | journal = N. Engl. J. Med. | volume = 343 | issue = 2 | pages = 78–85 | date = July 2000 | pmid = 10891514 | doi = 10.1056/NEJM200007133430201 }}</ref>
 
No single gene is responsible for prostate cancer; many different genes have been implicated. Mutations in ''[[BRCA1]]'' and ''[[BRCA2]]'', important risk factors for [[ovarian cancer]] and [[breast cancer]] in women, have also been implicated in prostate cancer.<ref name="pmid9145676">{{cite journal | author = Struewing JP, Hartge P, Wacholder S, Baker SM, Berlin M, McAdams M, Timmerman MM, Brody LC, Tucker MA | title = The risk of cancer associated with specific mutations of BRCA1 and BRCA2 among Ashkenazi Jews | journal = N. Engl. J. Med. | volume = 336 | issue = 20 | pages = 1401–8 | date = May 1997 | pmid = 9145676 | doi = 10.1056/NEJM199705153362001 }}</ref> Other linked genes include the [[RNASEL|Hereditary Prostate cancer gene 1]] (HPC1), the androgen receptor, and the [[vitamin D receptor]].<ref name="pmid9805030"/> [[TMPRSS2]]-[[ETS transcription factor family|ETS gene family]] [[fusion gene|fusion]], specifically TMPRSS2-[[ERG (gene)|ERG]] or TMPRSS2-[[ETV1]]/4 promotes cancer cell growth.<ref name="pmid19945666">{{cite journal | author = Beuzeboc P, Soulié M, Richaud P, Salomon L, Staerman F, Peyromaure M, Mongiat-Artus P, Cornud F, Paparel P, Davin JL, Molinié V | title = [Fusion genes and prostate cancer. From discovery to prognosis and therapeutic perspectives] | language = French | journal = Prog. Urol. | volume = 19 | issue = 11 | pages = 819–24 | date = December 2009 | pmid = 19945666 | doi = 10.1016/j.purol.2009.06.002 }}</ref>
 
Two large [[genome-wide association studies]] linking [[single nucleotide polymorphisms]] (SNPs) to prostate cancer were published in 2008.<ref>{{cite journal | author = Eeles RA, Kote-Jarai Z, Giles GG, Olama AA, Guy M, Jugurnauth SK, Mulholland S, Leongamornlert DA, Edwards SM, Morrison J, Field HI, Southey MC, Severi G, Donovan JL, Hamdy FC, Dearnaley DP, Muir KR, Smith C, Bagnato M, Ardern-Jones AT, Hall AL, O'Brien LT, Gehr-Swain BN, Wilkinson RA, Cox A, Lewis S, Brown PM, Jhavar SG, Tymrakiewicz M, Lophatananon A, Bryant SL, Horwich A, Huddart RA, Khoo VS, Parker CC, Woodhouse CJ, Thompson A, Christmas T, Ogden C, Fisher C, Jamieson C, Cooper CS, English DR, Hopper JL, Neal DE, Easton DF | title = Multiple newly identified loci associated with prostate cancer susceptibility | journal = Nature Genetics | volume = 40 | issue = 3 | pages = 316–21 | date = March 2008 | pmid = 18264097 | doi = 10.1038/ng.90 }}</ref><ref>{{cite journal | author = Thomas G, Jacobs KB, Yeager M, Kraft P, Wacholder S, Orr N, Yu K, Chatterjee N, Welch R, Hutchinson A, Crenshaw A, Cancel-Tassin G, Staats BJ, Wang Z, Gonzalez-Bosquet J, Fang J, Deng X, Berndt SI, Calle EE, Feigelson HS, Thun MJ, Rodriguez C, Albanes D, Virtamo J, Weinstein S, Schumacher FR, Giovannucci E, Willett WC, Cussenot O, Valeri A, Andriole GL, Crawford ED, Tucker M, Gerhard DS, Fraumeni JF, Hoover R, Hayes RB, Hunter DJ, Chanock SJ | title = Multiple loci identified in a genome-wide association study of prostate cancer | journal = Nature Genetics | volume = 40 | issue = 3 | pages = 310–5 | date = March 2008 | pmid = 18264096 | doi = 10.1038/ng.91 }}</ref> These studies identified several SNPs which substantially affect the risk of prostate cancer. For example, individuals with TT allele pair at SNP rs10993994 were reported to be at 1.6 times higher risk of prostate cancer than those with the CC allele pair. This SNP explains part of the increased prostate cancer risk of African American men as compared to American men of European descent, since the C allele is much more prevalent in the latter; this SNP is located in the promoter region of the ''MSMB'' gene, thus affects the amount of [[MSMB]] protein synthesized and secreted by epithelial cells of the prostate.<ref>{{cite journal | author = Whitaker HC, Kote-Jarai Z, Ross-Adams H, Warren AY, Burge J, George A, Bancroft E, Jhavar S, Leongamornlert D, Tymrakiewicz M, Saunders E, Page E, Mitra A, Mitchell G, Lindeman GJ, Evans DG, Blanco I, Mercer C, Rubinstein WS, Clowes V, Douglas F, Hodgson S, Walker L, Donaldson A, Izatt L, Dorkins H, Male A, Tucker K, Stapleton A, Lam J, Kirk J, Lilja H, Easton D, Cooper C, Eeles R, Neal DE | title = The rs10993994 risk allele for prostate cancer results in clinically relevant changes in microseminoprotein-beta expression in tissue and urine | journal = PLoS ONE | volume = 5 | issue = 10 | pages = e13363 | date = Oct 13, 2010 | pmid = 20967219 | pmc = 2954177 | doi = 10.1371/journal.pone.0013363 | editor1-last = Vickers | editor1-first = Andrew }} {{open access}}</ref>
 
===Dietary===
While some dietary factors have been associated with prostate cancer the evidence is still tentative.<ref>{{cite journal | author = Venkateswaran V, Klotz LH | title = Diet and prostate cancer: mechanisms of action and implications for chemoprevention | journal = Nature Reviews Urology | volume = 7 | issue = 8 | pages = 442–53 | date = Aug 2010 | pmid = 20647991 | doi = 10.1038/nrurol.2010.102 }}</ref> Evidence supports little role for dietary fruits and vegetables in prostate cancer occurrence.<ref>{{cite journal | author = Key TJ | title = Fruit and vegetables and cancer risk | journal = British journal of cancer | volume = 104 | issue = 1 | pages = 6–11 | year = 2011 | pmid = 21119663 | pmc = 3039795 | doi = 10.1038/sj.bjc.6606032 | quote = For other common cancers, including colorectal, breast and prostate cancer, epidemiological studies suggest little or no association between total fruit and vegetable consumption and risk. }}</ref> Red meat and processed meat also appear to have little effect in human studies.<ref>{{cite journal | author = Alexander DD, Mink PJ, Cushing CA, Sceurman B | title = A review and meta-analysis of prospective studies of red and processed meat intake and prostate cancer | journal = Nutrition journal | volume = 9 | issue =  | pages = 50 | year = 2010 | pmid = 21044319 | pmc = 2987772 | doi = 10.1186/1475-2891-9-50 }}</ref> Higher meat consumption has been associated with a higher risk in some studies.<ref>{{cite web|title=Chemicals in Meat Cooked at High Temperatures and Cancer Risk|url=http://www.cancer.gov/cancertopics/factsheet/Risk/cooked-meats|work=National Cancer Institute}}</ref>
 
Lower [[blood]] levels of [[vitamin D]] may increase the risk of developing prostate cancer.<ref>{{cite journal | author = Wigle DT, Turner MC, Gomes J, Parent ME | title = Role of hormonal and other factors in human prostate cancer | journal = Journal of Toxicology and Environmental Health. Part B, Critical Reviews | volume = 11 | issue = 3–4 | pages = 242–59 | date = March 2008 | pmid = 18368555 | doi = 10.1080/10937400701873548 }}</ref><!-- OFF TOPIC[[Green tea]] may be protective (due to its [[Tea catechins|catechins]] content),<ref name="pmid16613539">{{cite journal | author = Lee AH, Fraser ML, Meng X, Binns CW | title = Protective effects of green tea against prostate cancer | journal = Expert Rev Anticancer Ther | volume = 6 | issue = 4 | pages = 507–13 |date=April 2006 | pmid = 16613539 | doi = 10.1586/14737140.6.4.507 }}</ref> although the most comprehensive clinical study indicates that it has no protective effect.<ref name="pmid16804523">{{cite journal | author = Kikuchi N, Ohmori K, Shimazu T, Nakaya N, Kuriyama S, Nishino Y, Tsubono Y, Tsuji I | title = No association between green tea and prostate cancer risk in Japanese men: the Ohsaki Cohort Study | journal = Br. J. Cancer | volume = 95 | issue = 3 | pages = 371–3 |date=August 2006 | pmid = 16804523 | pmc = 2360636 | doi = 10.1038/sj.bjc.6603230 }}</ref> Other holistic methods are also studied.<ref name=Katz>{{Cite book|last=Katz |first=Aaron |authorlink=http://www.holisticurology.columbia.edu/_physicians/Katz.html |title=Guide to Prostate Health: From Conventional to Holistic Therapies |publisher=Freedom Press |year=2006 |isbn=1-893910-37-7}}</ref> Higher [[selenium]] blood levels have been associated with a lower risk of prostate cancer,<ref name="pmid22648711">{{cite journal | author = Hurst R, Hooper L, Norat T, Lau R, Aune D, Greenwood DC, Vieira R, Collings R, Harvey LJ, Sterne JA, Beynon R, Savović J, Fairweather-Tait SJ | title = Selenium and prostate cancer: systematic review and meta-analysis | journal = The American Journal of Clinical Nutrition | volume = 96 | issue = 1 | pages = 111–22 | year = 2012 | pmid = 22648711 | doi = 10.3945/ajcn.111.033373 }}</ref> a trial of supplementation however did not find benefit.<ref>{{cite book|last=Research|first=World Cancer Research Fund ; American Institute for Cancer|title=Policy and action for cancer prevention : food, nutrition, and physical activity : a global perspective|year=2007|publisher=American Institute for Cancer Research|location=Washington, D.C|isbn=978-0-9722522-4-9|pages=150}}</ref>-->
 
[[Folic acid]] [[Dietary supplement|supplements]] have no effect on the risk of developing prostate cancer.<ref>{{cite journal | author = Qin X, Cui Y, Shen L, Sun N, Zhang Y, Li J, Xu X, Wang B, Xu X, Huo Y, Wang X | title = Folic acid supplementation and cancer risk: A meta-analysis of randomized controlled trials | journal = International Journal of Cancer. Journal International Du Cancer | volume = 133 | issue = 5 | pages = 1033–41 | date = Jan 22, 2013 | pmid = 23338728 | doi = 10.1002/ijc.28038 }}</ref>
 
===Medication exposure===
There are also some links between prostate cancer and medications, medical procedures, and medical conditions.<ref name="pmid15998950">{{cite journal | author = Jacobs EJ, Rodriguez C, Mondul AM, Connell CJ, Henley SJ, Calle EE, Thun MJ | title = A large cohort study of aspirin and other nonsteroidal anti-inflammatory drugs and prostate cancer incidence | journal = J. Natl. Cancer Inst. | volume = 97 | issue = 13 | pages = 975–80 | date = July 2005 | pmid = 15998950 | doi = 10.1093/jnci/dji173 }}</ref> Use of the [[hypolipidaemic agent|cholesterol-lowering drugs]] known as the [[statin]]s may also decrease prostate cancer risk.<ref name="pmid16014776">{{cite journal | author = Shannon J, Tewoderos S, Garzotto M, Beer TM, Derenick R, Palma A, Farris PE | title = Statins and prostate cancer risk: a case-control study | journal = Am. J. Epidemiol. | volume = 162 | issue = 4 | pages = 318–25 | date = August 2005 | pmid = 16014776 | doi = 10.1093/aje/kwi203 }}</ref>
 
[[Infection]] or [[inflammation]] of the prostate ([[prostatitis]]) may increase the chance for prostate cancer while another study shows infection may help prevent prostate cancer by increasing blood to the area. In particular, infection with the [[sexually transmitted infection]]s [[Chlamydia infection|chlamydia]], [[gonorrhea]], or [[syphilis]] seems to increase risk.<ref name="pmid12100928">{{cite journal | author = Dennis LK, Lynch CF, Torner JC | title = Epidemiologic association between prostatitis and prostate cancer | journal = Urology | volume = 60 | issue = 1 | pages = 78–83 | date = July 2002 | pmid = 12100928 | doi = 10.1016/S0090-4295(02)01637-0 }}</ref> Finally, [[obesity]]<ref name="pmid12711737">{{cite journal | author = Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ | title = Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults | journal = N. Engl. J. Med. | volume = 348 | issue = 17 | pages = 1625–38 | date = April 2003 | pmid = 12711737 | doi = 10.1056/NEJMoa021423 }}</ref> and elevated blood levels of [[testosterone]]<ref name="pmid8757191">{{cite journal | author = Gann PH, Hennekens CH, Ma J, Longcope C, Stampfer MJ | title = Prospective study of sex hormone levels and risk of prostate cancer | journal = J. Natl. Cancer Inst. | volume = 88 | issue = 16 | pages = 1118–26 | date = August 1996 | pmid = 8757191 | doi = 10.1093/jnci/88.16.1118 }}</ref> may increase the risk for prostate cancer. There is an association between vasectomy and prostate cancer however more research is needed to determine if this is a causative relationship.<ref name="bccancer.bc.ca">{{cite web|url=http://www.bccancer.bc.ca |title=? |work= |publisher= |accessdate=9 August 2010}}</ref>
 
Research released in May 2007, found that US war veterans who had been exposed to [[Agent Orange]] had a 48% increased risk of prostate cancer recurrence following surgery.<ref name="aorange">{{cite web|url=https://my.mcg.edu/portal/page/portal/News/archive/2007/Veterans%20exposed%20to%20Agent%20%20Orange%20have%20higher%20rates%20of%20prost |title=Veterans exposed to Agent Orange have higher rates of prostate cancer recurrence |date=May 20, 2007 |work=Medical College of Georgia News }}</ref>
 
===Infectious disease===
An association with [[gonorrhea]] has been found, but a mechanism for this relationship has not been identified.<ref name="CainiGandini2014"/>
 
In 2006, a previously unknown retrovirus, [[Xenotropic MuLV-related virus]] or XMRV, was associated with human prostate tumors,<ref name="pmid16609730">{{cite journal | author = Urisman A, Molinaro RJ, Fischer N, Plummer SJ, Casey G, Klein EA, Malathi K, Magi-Galluzzi C, Tubbs RR, Ganem D, Silverman RH, DeRisi JL | title = Identification of a Novel Gammaretrovirus in Prostate Tumors of Patients Homozygous for R462Q RNASEL Variant | journal = PLoS Pathog. | volume = 2 | issue = 3 | pages = e25 | date = March 2006 | pmid = 16609730 | pmc = 1434790 | doi = 10.1371/journal.ppat.0020025 }} {{open access}}</ref> but subsequent reports on the virus were contradictory,<ref name="pmid19805305">{{cite journal | author = Schlaberg R, Choe DJ, Brown KR, Thaker HM, Singh IR | title = XMRV is present in malignant prostatic epithelium and is associated with prostate cancer, especially high-grade tumors | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 106 | issue = 38 | pages = 16351–6 | date = September 2009 | pmid = 19805305 | pmc = 2739868 | doi = 10.1073/pnas.0906922106 }}</ref><ref name="pmid19835577">{{cite journal | author = Hohn O, Krause H, Barbarotto P, Niederstadt L, Beimforde N, Denner J, Miller K, Kurth R, Bannert N | title = Lack of evidence for xenotropic murine leukemia virus-related virus (XMRV) in German prostate cancer patients | journal = Retrovirology | volume = 6 | issue =  | pages = 92 | year = 2009 | pmid = 19835577 | pmc = 2770519 | doi = 10.1186/1742-4690-6-92 }}</ref> and the original 2006 finding was instead due to a previously undetected contamination.<ref>{{cite journal | author = Lee D, Das Gupta J, Gaughan C, Steffen I, Tang N, Luk KC, Qiu X, Urisman A, Fischer N, Molinaro R, Broz M, Schochetman G, Klein EA, Ganem D, Derisi JL, Simmons G, Hackett J, Silverman RH, Chiu CY | title = In-Depth Investigation of Archival and Prospectively Collected Samples Reveals No Evidence for XMRV Infection in Prostate Cancer | journal = PLoS ONE | volume = 7 | issue = 9 | pages = e44954 | year = 2012 | pmid = 23028701 | pmc = 3445615 | doi = 10.1371/journal.pone.0044954 | editor1-last = Tachedjian | editor1-first = Gilda }} {{open access}}</ref> The journals ''Science'' and ''PlosONE'' both retracted XMRV related articles.<ref>{{cite journal | author = Alberts B | title = Retraction | journal = Science | volume = 334 | issue = 6063 | pages = 1636 | date = Dec 23, 2011 | pmid = 22194552 | doi = 10.1126/science.334.6063.1636-a }} {{open access}}</ref><ref>{{cite journal | title = Retraction. Identification of a novel gammaretrovirus in prostate tumors of patients homozygous for R462Q RNASEL variant | journal = PLoS Pathogens | volume = 8 | issue = 9 | pages = 10.1371/annotation/7e2efc01–2e9b–4e9b–aef0–87ab0e4e4732 | date = September 2012 | pmid = 23028303 | pmc = 3445601 | doi = 10.1371/annotation/7e2efc01-2e9b-4e9b-aef0-87ab0e4e4732 | editor1-last = Ross | editor1-first = Susan }} {{open access}}</ref>
 
===Sexual factors===
Several case-control studies have shown that having many lifetime sexual partners or starting sexual activity early in life substantially increases the risk of prostate cancer.<ref>{{cite journal | author = Dennis LK, Dawson DV | title = Meta-analysis of measures of sexual activity and prostate cancer | journal = Epidemiology (Cambridge, Mass.) | volume = 13 | issue = 1 | pages = 72–9 | date = January 2002 | pmid = 11805589 | doi = 10.1097/00001648-200201000-00012 }}</ref><ref name="Rosenblatt 1152–8">{{cite journal | author = Rosenblatt KA, Wicklund KG, Stanford JL | title = Sexual factors and the risk of prostate cancer | journal = American Journal of Epidemiology | volume = 153 | issue = 12 | pages = 1152–8 | date = Jun 15, 2001 | pmid = 11415949 | doi = 10.1093/aje/153.12.1152 }}</ref><ref>{{cite journal | author = Sarma AV, McLaughlin JC, Wallner LP, Dunn RL, Cooney KA, Schottenfeld D, Montie JE, Wei JT | title = Sexual behavior, sexually transmitted diseases and prostatitis: the risk of prostate cancer in black men | journal = The Journal of Urology | volume = 176 | issue = 3 | pages = 1108–13 | date = September 2006 | pmid = 16890703 | doi = 10.1016/j.juro.2006.04.075 }}</ref>
 
While the available evidence is weak,<ref>{{cite book|title=Male Reproductive Cancers|year=2010|publisher=Springer New York|isbn=9781441904508|pages=27|url=https://books.google.com/books?id=mAYPxgOoBK4C&pg=PA27}}</ref> tentative results suggest that frequent [[ejaculation]] may decrease the risk of prostate cancer.<ref>{{cite book|last=Scardino|first=Peter|title=Comprehensive textbook of genitourinary oncology|year=2005|publisher=Lippincott Williams & Wilkins|location=Philadelphia|isbn=9780781749848|pages=16|url=https://books.google.com/books?id=jaLRxFFEwNsC&pg=PA16|edition=3rd}}</ref> A study, over eight years, showed that those that ejaculated most frequently (over 21 times per month on average) were less likely to get prostate cancer.<ref>{{cite journal|last1=Leitzmann|first1=MF|last2=Platz|first2=EA|last3=Stampfer
|first3=MJ|last4=Willett|first4=WC|last5=Giovannucci|first5=E|title=Ejaculation frequency and subsequent risk of prostate cancer.|journal=JAMA|date=7 April 2004|volume=291|issue=13|pages=1578–86|pmid=15069045|doi=10.1001/jama.291.13.1578}}</ref> The results were broadly similar to the findings of a smaller Australian study.<ref>{{cite journal|last1=Giles|first1=GG|last2=Severi |first2=G|last3=English|first3=DR|last4=McCredie |first4=MR|last5=Borland|first5=R|last6=Boyle|first6=P|last7=Hopper|first7=JL|title=Sexual factors and prostate cancer.|journal=BJU international|date=August 2003|volume=92|issue=3|pages=211–6|pmid=12887469|doi=10.1046/j.1464-410x.2003.04319.x}}</ref>
 


==References==
==References==

Revision as of 19:22, 15 September 2015

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Overview

Common risk factors in the development of prostate cancer are dietary, lifestyle, family history, African-American men, occupational factors, age, environmental factors, and medication.

Risk Factors

Common risk factors in the development of prostate cancer include:

Genetic

Genetic background may contribute to prostate cancer risk, as suggested by associations with race, family, and specific gene variants. Men who have a first-degree relative (father or brother) with prostate cancer have twice the risk of developing prostate cancer, and those with two first-degree relatives affected have a fivefold greater risk compared with men with no family history.[1] In the United States, prostate cancer more commonly affects black men than white or Hispanic men, and is also more deadly in black men.[2][3] In contrast, the incidence and mortality rates for Hispanic men are one third lower than for non-Hispanic whites. Studies of twins in Scandinavia suggest that 40% of prostate cancer risk can be explained by inherited factors.[4]

No single gene is responsible for prostate cancer; many different genes have been implicated. Mutations in BRCA1 and BRCA2, important risk factors for ovarian cancer and breast cancer in women, have also been implicated in prostate cancer.[5] Other linked genes include the Hereditary Prostate cancer gene 1 (HPC1), the androgen receptor, and the vitamin D receptor.[2] TMPRSS2-ETS gene family fusion, specifically TMPRSS2-ERG or TMPRSS2-ETV1/4 promotes cancer cell growth.[6]

Two large genome-wide association studies linking single nucleotide polymorphisms (SNPs) to prostate cancer were published in 2008.[7][8] These studies identified several SNPs which substantially affect the risk of prostate cancer. For example, individuals with TT allele pair at SNP rs10993994 were reported to be at 1.6 times higher risk of prostate cancer than those with the CC allele pair. This SNP explains part of the increased prostate cancer risk of African American men as compared to American men of European descent, since the C allele is much more prevalent in the latter; this SNP is located in the promoter region of the MSMB gene, thus affects the amount of MSMB protein synthesized and secreted by epithelial cells of the prostate.[9]

Dietary

While some dietary factors have been associated with prostate cancer the evidence is still tentative.[10] Evidence supports little role for dietary fruits and vegetables in prostate cancer occurrence.[11] Red meat and processed meat also appear to have little effect in human studies.[12] Higher meat consumption has been associated with a higher risk in some studies.[13]

Lower blood levels of vitamin D may increase the risk of developing prostate cancer.[14]

Folic acid supplements have no effect on the risk of developing prostate cancer.[15]

Medication exposure

There are also some links between prostate cancer and medications, medical procedures, and medical conditions.[16] Use of the cholesterol-lowering drugs known as the statins may also decrease prostate cancer risk.[17]

Infection or inflammation of the prostate (prostatitis) may increase the chance for prostate cancer while another study shows infection may help prevent prostate cancer by increasing blood to the area. In particular, infection with the sexually transmitted infections chlamydia, gonorrhea, or syphilis seems to increase risk.[18] Finally, obesity[19] and elevated blood levels of testosterone[20] may increase the risk for prostate cancer. There is an association between vasectomy and prostate cancer however more research is needed to determine if this is a causative relationship.[21]

Research released in May 2007, found that US war veterans who had been exposed to Agent Orange had a 48% increased risk of prostate cancer recurrence following surgery.[22]

Infectious disease

An association with gonorrhea has been found, but a mechanism for this relationship has not been identified.[23]

In 2006, a previously unknown retrovirus, Xenotropic MuLV-related virus or XMRV, was associated with human prostate tumors,[24] but subsequent reports on the virus were contradictory,[25][26] and the original 2006 finding was instead due to a previously undetected contamination.[27] The journals Science and PlosONE both retracted XMRV related articles.[28][29]

Sexual factors

Several case-control studies have shown that having many lifetime sexual partners or starting sexual activity early in life substantially increases the risk of prostate cancer.[30][31][32]

While the available evidence is weak,[33] tentative results suggest that frequent ejaculation may decrease the risk of prostate cancer.[34] A study, over eight years, showed that those that ejaculated most frequently (over 21 times per month on average) were less likely to get prostate cancer.[35] The results were broadly similar to the findings of a smaller Australian study.[36]


References

  1. ↑ Steinberg GD, Carter BS, Beaty TH, Childs B, Walsh PC (1990). "Family history and the risk of prostate cancer". Prostate. 17 (4): 337–47. doi:10.1002/pros.2990170409. PMID 2251225.
  2. ↑ 2.0 2.1 Gallagher RP, Fleshner N (October 1998). "Prostate cancer: 3. Individual risk factors" (PDF). CMAJ. 159 (7): 807–13. PMC 1232741. PMID 9805030.
  3. ↑ Hoffman RM, Gilliland FD, Eley JW, Harlan LC, Stephenson RA, Stanford JL, Albertson PC, Hamilton AS, Hunt WC, Potosky AL (March 2001). "Racial and ethnic differences in advanced-stage prostate cancer: the Prostate Cancer Outcomes Study". J. Natl. Cancer Inst. 93 (5): 388–95. doi:10.1093/jnci/93.5.388. PMID 11238701.
  4. ↑ Lichtenstein P, Holm NV, Verkasalo PK, Iliadou A, Kaprio J, Koskenvuo M, Pukkala E, Skytthe A, Hemminki K (July 2000). "Environmental and heritable factors in the causation of cancer--analyses of cohorts of twins from Sweden, Denmark, and Finland". N. Engl. J. Med. 343 (2): 78–85. doi:10.1056/NEJM200007133430201. PMID 10891514.
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  26. ↑ Hohn O, Krause H, Barbarotto P, Niederstadt L, Beimforde N, Denner J, Miller K, Kurth R, Bannert N (2009). "Lack of evidence for xenotropic murine leukemia virus-related virus (XMRV) in German prostate cancer patients". Retrovirology. 6: 92. doi:10.1186/1742-4690-6-92. PMC 2770519. PMID 19835577.
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  33. ↑ Male Reproductive Cancers. Springer New York. 2010. p. 27. ISBN 9781441904508.
  34. ↑ Scardino, Peter (2005). Comprehensive textbook of genitourinary oncology (3rd ed.). Philadelphia: Lippincott Williams & Wilkins. p. 16. ISBN 9780781749848.
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  36. ↑ Giles, GG; Severi, G; English, DR; McCredie, MR; Borland, R; Boyle, P; Hopper, JL (August 2003). "Sexual factors and prostate cancer". BJU international. 92 (3): 211–6. doi:10.1046/j.1464-410x.2003.04319.x. PMID 12887469.

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