Early prostate cancer usually has no clear symptoms. Sometimes,
however, prostate cancer does cause symptoms, often similar to those of
diseases such as benign prostatic hyperplasia. These include frequent urination, nocturia (increased urination at night), difficulty starting and maintaining a steady stream of urine, hematuria (blood in the urine), and dysuria
(painful urination). A study based on the 1998 Patient Care Evaluation
in the US found that about a third of patients diagnosed with prostate
cancer had one or more such symptoms, while two thirds had no symptoms.[13]
Prostate cancer is associated with urinary dysfunction as the prostate gland surrounds the prostatic urethra. Changes within the gland, therefore, directly affect urinary function. Because the vas deferens deposits seminal fluid into the prostatic urethra, and secretions from the prostate gland itself are included in semen content, prostate cancer may also cause problems with sexual function and performance, such as difficulty achieving erection or painful ejaculation.[13]
Advanced prostate cancer can spread to other parts of the body, possibly causing additional symptoms. The most common symptom is bone pain, often in the vertebrae (bones of the spine), pelvis, or ribs. Spread of cancer into other bones such as the femur is usually to the proximal or nearby part of the bone. Prostate cancer in the spine can also compress the spinal cord, causing tingling, leg weakness and urinary and fecal incontinence.[14]
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.[27] Other linked genes include the Hereditary Prostate cancer gene 1 (HPC1), the androgen receptor, and the vitamin D receptor.[24] TMPRSS2-ETS gene family fusion, specifically TMPRSS2-ERG or TMPRSS2-ETV1/4 promotes cancer cell growth.[28]
Two large genome-wide association studies linking single nucleotide polymorphisms (SNPs) to prostate cancer were published in 2008.[29][30] 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.[31]
Lower blood levels of vitamin D may increase the risk of developing prostate cancer.[36]
Folic acid supplements have no effect on the risk of developing prostate cancer.[37]
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.[40] Finally, obesity[41] and elevated blood levels of testosterone[42] 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.[43]
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.[44]
In 2006, a previously unknown retrovirus, Xenotropic MuLV-related virus or XMRV, was associated with human prostate tumors,[45] but subsequent reports on the virus were contradictory,[46][47] and the original 2006 finding was instead due to a previously undetected contamination.[48] The journals Science and PlosONE both retracted XMRV related articles.[49][50]
While the available evidence is weak,[54] tentative results suggest that frequent ejaculation may decrease the risk of prostate cancer.[55] 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.[56] The results were broadly similar to the findings of a smaller Australian study.[57]
Prostate cancer is associated with urinary dysfunction as the prostate gland surrounds the prostatic urethra. Changes within the gland, therefore, directly affect urinary function. Because the vas deferens deposits seminal fluid into the prostatic urethra, and secretions from the prostate gland itself are included in semen content, prostate cancer may also cause problems with sexual function and performance, such as difficulty achieving erection or painful ejaculation.[13]
Advanced prostate cancer can spread to other parts of the body, possibly causing additional symptoms. The most common symptom is bone pain, often in the vertebrae (bones of the spine), pelvis, or ribs. Spread of cancer into other bones such as the femur is usually to the proximal or nearby part of the bone. Prostate cancer in the spine can also compress the spinal cord, causing tingling, leg weakness and urinary and fecal incontinence.[14]
Risk factors
A complete understanding of the causes of prostate cancer remains elusive.[15] The primary risk factors are obesity, age and family history. 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.[16] 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 30% of men in their 50s, and in 80% of men in their 70s.[17] Men who have first-degree family members with prostate cancer appear to have double the risk of getting the disease compared to men without prostate cancer in the family.[18] This risk appears to be greater for men with an affected brother than for men with an affected father. 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.[19] Men with high blood pressure are more likely to develop prostate cancer.[20] There is a small increased risk of prostate cancer associated with lack of exercise.[21] A 2010 study found that prostate basal cells were the most common site of origin for prostate cancers.[22]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.[23] In the United States, prostate cancer more commonly affects black men than white or Hispanic men, and is also more deadly in black men.[24][25] 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.[26]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.[27] Other linked genes include the Hereditary Prostate cancer gene 1 (HPC1), the androgen receptor, and the vitamin D receptor.[24] TMPRSS2-ETS gene family fusion, specifically TMPRSS2-ERG or TMPRSS2-ETV1/4 promotes cancer cell growth.[28]
Two large genome-wide association studies linking single nucleotide polymorphisms (SNPs) to prostate cancer were published in 2008.[29][30] 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.[31]
Dietary
While some dietary factors have been associated with prostate cancer the evidence is still tentative.[32] Evidence supports little role for dietary fruits and vegetables in prostate cancer occurrence.[33] Red meat and processed meat also appear to have little effect in human studies.[34] Higher meat consumption has been associated with a higher risk in some studies.[35]Lower blood levels of vitamin D may increase the risk of developing prostate cancer.[36]
Folic acid supplements have no effect on the risk of developing prostate cancer.[37]
Medication exposure
There are also some links between prostate cancer and medications, medical procedures, and medical conditions.[38] Use of the cholesterol-lowering drugs known as the statins may also decrease prostate cancer risk.[39]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.[40] Finally, obesity[41] and elevated blood levels of testosterone[42] 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.[43]
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.[44]
Infectious disease
An association with gonorrhea has been found, but a mechanism for this relationship has not been identified.[6]In 2006, a previously unknown retrovirus, Xenotropic MuLV-related virus or XMRV, was associated with human prostate tumors,[45] but subsequent reports on the virus were contradictory,[46][47] and the original 2006 finding was instead due to a previously undetected contamination.[48] The journals Science and PlosONE both retracted XMRV related articles.[49][50]
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.[51][52][53]While the available evidence is weak,[54] tentative results suggest that frequent ejaculation may decrease the risk of prostate cancer.[55] 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.[56] The results were broadly similar to the findings of a smaller Australian study.[57]
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