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  Oct 22, 2018
Prostate Cancer and Genetics
Prostate Cancer and Genetics
  Oct 22, 2018

The actual cause of prostate cancer is not known. However, studies have shown that individuals of certain ethnicities such as Afro-Caribbeans and African Americans have an increased risk of developing this cancer, while Asian individuals have a decreased risk of developing it. Prostate cancer also seems to run in families, with individuals at a greater risk for the condition if they have a first-degree relative such as a brother or father who has had prostate cancer. Together, these facts suggest that genetics may play a role in the development of this condition.

Genetic studies have revealed several inheritable gene mutations that are associated with an increased risk for prostate cancer. Genes, however, may only play a small role in causing this condition. Genetic testing for these mutations is not yet available and further studies are needed to confirm whether such tests could be valuable predictors of prostate cancer.

Genes that may be implicated in prostate cancer

Some inherited gene mutations are associated with an increased risk of more than one cancer type. For example, the inheritance of abnormal BRCA1 or BRCA2 genes accounts for an increased risk for breast and ovarian cancer in some families. Studies have shown that mutations of these genes may also raise the risk of prostate cancer in men, although only in a small number of cases.

Mutations in certain other genes have been identified as causative factors in around 5% to 10% of all prostate cancers. One examples is the HPC1 (Hereditary Prostate Cancer Gene 1) gene, but many other gene alterations that potentially play a role in the inherited tendency towards this condition are being studied.

A mutation is a change or abnormality in the DNA of a cell that causes abnormal cell growth and the proliferation of more abnormal cells. These abnormal cells do not die or get killed off as would usually be the case when a cell is worn out or damaged in some way. DNA mutations can activate genes called oncogenes that instruct cells to divide and proliferate. They can also deactivate genes called tumor suppressor genes, which cause apoptosis or cell death.