Prostate cancer is the most common type of cancer that affects human males. It is often asymptomatic and develops over a long period of time. Nearly 750,000 men are diagnosed with prostate cancer every year. Interestingly the incidence is highest in Scandinavia, Western Europe and North America, and lowest in South and East Asia. This suggests a strong genetic component to cancer susceptibility.

However, contrary to this finding, and in common with other cancers, a virus has recently been associated with the most severe forms of prostate cancer.

In September 2009, researchers from Utah discovered that the Xenotropic murine leukaemia virus (XMRV) was found in 27% of the 200 prostate cancer cases investigated. The virus seems to associate itself with the most aggressive tumours. This important discovery could lead to the production of a vaccine based upon an anti-viral antibody, as is the case with Cervical cancer and Human Papilloma Virus.

What is interesting is that the virus has an androgen response element and seems to grow better in the presence of testosterone. This could be a very important step towards understanding how the cancer is triggered and subsequently, how it can be controlled.

A major XMRV integration site has been mapped to a gene encoding a suppressor of androgen receptor transactivation (APPBP2). It can be hypothesised that upon XMRV infection, androgen receptor transactivation is increased by the blocking of APPBP2, which could be the trigger for cancer. Comparing the sequence of APPBP2 to XMRV using SynaCompare identifies two short domains which are highly homologous and could be the sites of insertion, leading to the disruption of the protein.

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Click here, then click on .
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On the results page, click on to view thick lines.
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Two short homologous domains can be seen.

Right click and move cursor to select region and click inside selected region to zoom in.

It can be hypothesized that these homologous regions could be the sites of insertion, leading to the disruption of the protein.
Source : BBC News.

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