The specific causes of prostate cancer remain unknown. A man's risk of developing prostate cancer is related to his age, genetics, race, diet, lifestyle, medications, and other factors. The primary risk factor is age. Prostate cancer is very uncommon in men younger than 45, but becomes more common with advancing age. The average age at the time of diagnosis is 70. However, many men never know they have prostate cancer. Autopsy studies of Chinese, German, Israeli, Jamaican, Swedish, and Ugandan men who died of other causes have found prostate cancer in thirty percent of men in their 50s, and in eighty percent of men in their 70s. In the United States in 2005, there were an estimated 230,000 new cases of prostate cancer and 30,000 deaths due to prostate cancer. Men with high blood pressure are more likely to develop prostate cancer.
Genetics
Genetic background may contribute to prostate cancer risk, as suggested by associations with race, family, and specific gene variants.Men with one first-degree relatives with prostate cancer have a twofold higher risk,and those with two first-degree relatives have a fivefold greater risk of developing prostate cancer compared with men with no family history.In the United States, prostate cancer more commonly affects black men than white or Hispanic men, and is also more deadly in black men. In contrast, the incidence and mortality rates for Hispanic men are one third lower than for non-Hispanic whites. Men who have a brother or father with prostate cancer have twice the risk of developing prostate cancer. Studies of twins in Scandinavia suggest that forty percent of prostate cancer risk can be explained by inherited factors.
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. Other linked genes include the Hereditary Prostate cancer gene-1"HPC1"(mapped to chromosome 1q24-25), the androgen receptor, and the vitamin D receptor. TMPRSS2-ETS gene family fusion, specifically TMPRSS2/ERG or TMPRSS2/ETV1/4 promotes cancer cell growth. Loss of cancer suppressor genes,early in the prostatic carcinogenesis, have been localized to chromosomes 8p, 10q, 13q,and 16q .p53 mutations in the primary prostate cancer are relatively low and are more frequently seen in Metastatic settings,hence, p53 mutations are late event in pathology of prostate cancer.Other tumor suppressor genes that are thought to play a role in prostate cancer include PTEN (gene) and KAI1.Relative frequency of loss of E-cadherin and CD44 has also been observed.
Diet
Evidence from epidemiological studies supports a possible protective role in reducing prostate cancer for dietary Vitamin B6, selenium, vitamin E, lycopene, and soy foods. A study in 2007 cast doubt on the effectiveness of lycopene (found in tomatoes) in reducing the risk of prostate cancer. Lower blood levels of vitamin D may increase the risk of developing prostate cancer. This may be linked to lower exposure to ultraviolet (UV) light, since UV light exposure can increase vitamin D in the body.
Studies comparing men who live in areas of the country with high levels of selenium to men in areas with low levels suggest that this mineral protects against prostate cancer. Selenium is believed to reduce the risk of developing prostate cancer because it keeps cells from proliferating or dying off in a rapid or unusual way. An analysis in 2002 of the Nutritional Prevention of Cancer Trial revealed that the men who took selenium supplements daily were half as likely to be diagnosed with prostate cancer. However, in 2008, the Selenium and Vitamin E Cancer Prevention Trial (SELECT) indicated that neither selenium nor vitamin E, alone or in combination, was effective for the primary prevention of prostate cancer. Whether or not selenium helps prevent prostate cancer, researchers at the Dana-Farber Cancer Institute in Boston found that higher selenium levels in the blood may worsen prostate cancer in many men who already have the disease.
Green tea may be protective (due to its polyphenol content), although the most comprehensive clinical study indicates that it has no protective effect.
Research published in the Journal of the National Cancer Institute suggests that taking multivitamins more than seven times a week can increase the risks of contracting the disease. This research was unable to highlight the exact vitamins responsible for this increase (almost double), although they suggest that vitamin A, vitamin E and beta-carotene may lie at its heart. It is advised that those taking multivitamins never exceed the stated daily dose on the label.
A 2007 study published in the Journal of the National Cancer Institute found that men eating cauliflower, broccoli, or one of the other cruciferous vegetables, more than once a week were 40% less likely to develop prostate cancer than men who rarely ate those vegetables. The phytochemicals indole-3-carbinol and diindolylmethane, found in cruciferous vegetables, has antiandrogenic and immune modulating properties.
Many doctors prescribe supplements to prostate cancer patients but currently the efficacy of nutrient supplements is still unknown. Supplements may not be as beneficial to prostate health as micronutrients obatined naturally from the diet.
Folic acid supplements have recently been linked to an increase in risk of developing prostate cancer. A ten-year research study led by University of Southern California researchers showed that men who took daily folic acid supplements of 1 mg were three times more likely to be diagnosed with prostate cancer than men who took a placebo. Folate plays a complex role in prostate cancer and folic acid supplements have a different effect on prostate cancer than folate naturally found in foods. The supplement form, folic acid, is more bioavailable in the body compared with dietary sources of folate. Folate hydrolase activity is associated with prostate-specific antigen. A small Swedish study of 254 subjects, with a median age of 64, and a follow up of 5 years suggested that folate status is not protective against prostate cancer, however, and like folic acid may even result in a 3 fold increase in early prostate cancer development and risk. Supplements and multivitamins, alcohol and drug consumption, GI disorders, and folate bioavailability were not analyzed in this study.
High alcohol intake may increase the risk of prostate cancer and interfere with folate metabolism. Low folate intake and high alcohol intake may increase the risk of prostate cancer to a greater extent than the sole effect of either one by itself. A case control study consisting of 137 veterans addressed this hypothesis and the results were that high folate intake was related to a 79% lower risk of developing prostate cancer and there was no association between alcohol consumption by itself and prostate cancer risk. Folate's effect however was only significant when coupled with low alcohol intake. There is a significant decrease in risk of prostate cancer with increasing dietary folate intake but this association only remains in individuals with low levels of alcohol consumption. There was no association found in this study between folic acid supplements and risk of prostate cancer.
The prostate gland has a high concentration of zinc so it has been hypothesized that zinc plays a role in prostate cancer. Recently researchers studied the relationship between zinc supplement intake of 100 mg/day and the risk of prostate cancer in 46 974 US men over a 14 year period and found that long term zinc supplement intake may play a role in prostate carcinogenesis.
Medication exposure
There are also some links between prostate cancer and medications, medical procedures, and medical conditions. Daily use of anti-inflammatory medicines such as aspirin, ibuprofen, or naproxen may decrease prostate cancer risk. Use of the cholesterol-lowering drugs known as the statins may also decrease prostate cancer risk. Infection or inflammation of the prostate (prostatitis) may increase the chance for prostate cancer. In particular, infection with the sexually transmitted infections chlamydia, gonorrhea, or syphilis seems to increase risk. Finally, obesity and elevated blood levels of testosterone 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.
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.
Potential viral cause
In 2006, researchers associated a previously unknown retrovirus, Xenotropic MuLV-related virus or XMRV, with human prostate tumors. Subsequent reports on the virus have been contradictory. A group of US researchers found XMRV protein expression in human prostate tumors, while German scientists failed to find XMRV-specific antibodies or XMRV-specific nucleic acid sequences in prostate cancer samples.
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