2 September 2011
Genetic mutations in the breast cancer susceptibility one gene (BRCA1) that cause excessive DNA repair could also contribute to cancer development, researchers claim.
Prior opinion held that it was just reductions in the DNA repair which actually caused cancerous cells to develop, but research carried out at the Virginia Commonwealth University and published in the Aging journal has challenged this view.
Researchers, led by Dr Kristoffer Valerie, found that excessive repair activity, while not the causer of cancer, certainly indicated a faultering repair process in which cancer could develop, potentially carrying major implications for the future development of cancer treatment.
"Our findings suggest that caution should be exercised when targeting BRCA1 for breast and ovarian cancer therapies," Dr Valerie, professor in the Department of Radiation Oncology at Virginia, claimed.
In other genetic discoveries behind cancer development, findings published in the Science Translation Journal on Wednesday (August 31st) claimed to have uncovered a rare genetic alteration behind a form of blood cancer known as epithelioid hemangioendothelioma (or EHE).
Posted by Edward Bartel
1 Dever, Seth M., et. al., Mutations in the BRCT binding site of BRCA1 result in hyper-recombination". Aging. August 5th 2011.
2 Tanas, Munir R., et. al., "Identification of a Disease-Defining Gene Fusion in Epithelioid Hemangioendothelioma". Science Translational Medicine. Wednesday August 31st 2011.
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