A Japanese-U.S. study suggested that a mechanism that repairs damaged DNA might malfunction and result in breast cancer.

   Although defects in the "breast cancer gene" BRCA1 have been known for years to increase the risk of breast cancer, exactly how it leads to tumor growth hasn't been determined.

   In the new research, medical scientists from the University of Chicago and Kyoto University provide insight into how the normal BRCA1 gene suppresses the growth of tumors, as well as the nature of the genetic instability that leads to cancer when BRCA1 is defective.

   "If you take a normal, healthy cell and get rid of BRCA1, you end up with an unhealthy, slow-growing cell," said Associate Professor Douglas Bishop of the University of Chicago, principal investigator of the study. "That's a bit of a paradox, because loss of BRCA1 also causes tumors and tumor formation is not normally associated with poor cell growth."

   BRCA1 itself promotes DNA repair through recombination and the conventional view is that loss of BRCA1 causes tumors because DNA repair fails. The new work from Bishop and colleagues challenges that view.

   The study is reported in the journal Cancer Research.

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