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Our own treacherous immune genes can cause cancer after viral infection
Date:6/5/2014

dly fire' more likely. Alternatively, there may well be something about the virus that causes the APOBEC response to wrongly target the body's own genes for mutation."

Mutated PIK3CA (p110α) protein is known to play a key role in the development of a range of cancers, so it is a hot target for new drugs. The new research could explain why particular PIK3CA mutation variants are so commonly found in HPV-associated cancers.

"While it is too early to consider targeting APOBEC genes to prevent tumour formation, it is nonetheless fascinating to work out how HPV drives tumour formation through their activity," says co-lead author Ankur Chakravarthy, a PhD student in the Tumour Virus team. The team's aim is now to learn what happens following HPV infection of cells in which APOBEC genes have been deleted.

The research could also inform screening procedures, as there are variants of particular APOBEC genes that are known to affect cancer risk. For example, a variant of the specific gene APOBEC3B is known to approximately double breast cancer risk. This variant is common in East Asia, with approximately 80% of Indonesians carrying the gene variant. By contrast, only around 2% of the African population carry this variant.

"Previous studies have shown that APOBECs cause mutations in a range of cancers but our finding that they mutate key cancer genes implicates them as drivers of tumour development, particularly in HPV-associated cancers. It will be interesting to see whether such APOBEC variants can predict the risk of developing cancer after HPV infections," says Dr Tim Fenton. "If at-risk groups could be identified by genetic testing, this could have important implications for HPV screening and vaccination programmes."


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Contact: Harry Dayantis
h.dayantis@ucl.ac.uk
44-020-310-83844
University College London
Source:Eurekalert

Page: 1 2

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