What Is Prostate Cancer?

Prostate cancer is a disease which only affects men. Cancer begins to grow in the prostate - a gland in the male reproductive system. The prostate is an exocrine gland of the male reproductive system, and exists directly under the bladder, in front of the rectum. An exocrine gland is one whose secretions end up outside the body e.g. prostate gland and sweat glands. It is approximately the size of a walnut. The urethra - a tube that goes from the bladder to the end of the penis and carries urine and semen out of the body - goes through the prostate. In the vast majority of cases, the prostate cancer starts in the gland cells - this is called adenocarcinoma. In this article, prostate cancer refers just to adenocarcinoma. Prostate cancer is mostly a very slow progressing disease. In fact, many men die of old age, without ever knowing they had prostate cancer - it is only when an autopsy is done that doctors know it was there. Several studies have indicated that perhaps about 80% of all men in their eighties had prostate cancer when they died, but nobody knew, not even the doctor.

What are prostate cancer causes?

The risk (predisposing) factors for prostate cancer include advancing age, genetics (heredity), hormonal influences, and such environmental factors as toxins, chemicals, and industrial products. Genetics (heredity), as just mentioned, plays a role in the risk of developing a prostate cancer. Prostate cancer is more common among family members of individuals with prostate cancer. This risk may be two to three times greater than the risk for men without a family history of the disease. Earlier age at diagnosis (< 60 years) in a first-degree relative (father or brother) and disease affecting more than one relative also increases the risk for developing prostate cancer.

ELAC2 polymorphisms and prostate cancer risk.

Polymorphisms in the elaC homolog-2 (ELAC2)/HPC2 gene have been hypothesized to alter the risk of prostate cancer. ELAC2 was thought to serve as a metal-dependent hydrolase and to be potentially involved in DNA inter-strand crosslink repair and mRNA editing. Moreover, the human ELAC2 protein was shown to possess 3'-tRNase activity and to interact with ?-tubulin, a component of the mitotic apparatus, suggesting a possible role for ELAC2 in the regulation of cell-cycle progression. The ELAC2 Ser217Leu and Ala541Thr polymorphisms might be associated with prostate cancer risk.

Androgen Receptor Gene.

Androgen receptor (AR) gene variants have been examined in relation to both prostate cancer risk and disease progression. The AR is expressed during all stages of prostate carcinogenesis. Androgen receptor (AR) gene variants have been examined in relation to both prostate cancer risk and disease progression. The AR is expressed during all stages of prostate carcinogenesis. Altered activity of the AR due to inherited variants of the AR gene may influence risk of prostate cancer. The length of the polymorphic trinucleotide CAG and GGN microsatellite repeats in exon 1 of the AR gene (located on the X chromosome) have been associated with the risk of prostate cancer.

5-Alpha-Reductase Gene (SRD5A2).

Molecular epidemiology studies have also examined genetic polymorphisms of the 5-alpha-reductase type II gene, which is also involved in the androgen metabolism cascade. Two isozymes of 5-alpha-reductase exist. The gene that codes for 5-alpha-reductase type II (SRD5A2) is located on chromosome 2. It is expressed in the prostate, where testosterone is converted irreversibly to dihydroxytestosterone (DHT) by 5-alpha-reductase type II. Evidence suggests that 5-alpha-reductase type II activity is reduced in populations at lower risk of prostate cancer, including Chinese and Japanese men.A polymorphism in the untranslated region of the SRD5A2 gene may also be associated with prostate cancer risk.

Toll-like Receptor Genes.

The family of toll-like receptors has been recognized as a critical component of the intrinsic immune system, one which recognizes ligands from exogenous microbes and a variety of endogenous substrates. This family of genes has been studied most extensively in the context of autoimmune disease, but there also have been a series of studies that have analyzed genetic variants in various members of this pathway as potential prostate cancer risk modifiers. SNPs in a region on chromosome 4p14 that includes TLR-10, TLR-1 and TLR-6, three members of the toll-like receptor gene cluster. Two TLR-10 SNPs and four TLR-1 SNPs were associated with significant reductions in prostate cancer risk, ranging from 29% to 38% for the homozygous variant genotype.

Vitamin D receptor gene.

Higher vitamin D exposure is hypothesized to prevent several cancers, possibly through genomic effects modulated by the vitamin D receptor (VDR). polymorphisms in VDR and selected genes in the vitamin D pathway has associations in prostate cancer. . Although most studies to date have examined only a few VDR polymorphisms, more are beginning to comprehensively investigate polymorphisms in the VDR as well as in other vitamin D pathway genes, such as the vitamin D–binding protein gene (Gc) and CYP27B1 and CYP24A1, which code for enzymes that, respectively, synthesize and degrade 1a,25-(OH)2-vitamin D. Currently, there is no strong, consistent epidemiologic evidence for substantial influences of single variants in vitamin D pathway genes on risk for prostate cancer, but promising leads are developing.

E-Cadherin Gene.

E-cadherin is a tumor suppressor gene. . A SNP designated -160?A, located in the promoter region of E-cadherin, has been found to alter the transcriptional activity of this gene.

Estrogen Receptor-Beta Gene.

SNP in the promoter region of ER-beta, rs2987983, was associated with an overall prostate cancer risk

Polymorphism In Endostatin.

Endostatin is a cleavage product of collagen and is a potent inhibitor of endothelial cell proliferation and migration. Endostatin causes apoptosis in endothelial and tumor cells. Prostate cancer expresses angiogenic factors. A missense mutation in the coding region for endostatin has been described, but the polymorphism affects protein conformation rather than protein expression. Cellular assays suggested that the result is impaired endostatin binding to laminin, a basement membrane protein. D104N endostatin polymorphism in relation to prostate cancer risk and survival.