Deviation of a tumor suppressing gene has been found to be associated with ovarian cancer. The cancerous cells are said to be the result of an endometriosis turning into cancer. Two different studies have reported similar facts where the mutated form of the gene ARID1A was found in 50% of all clear cell ovarian carcinomas. The results of one of the studies have also reported finding the particular gene in 30% of all endometrioid carcinomas with none being obvious in serious cases of ovarian cancer.
An abnormal chromatin remodeling has been held responsible by the researchers involved in both the studies. This is being considered as the primary factor for the development of cancer from endometriosis.
David G. Huntsman, MD, author of the online publication of the study result in the New England Journal of Medicine, said that the mutations of the gene ARID1A along with the loss of the BAF250a expressions in the tumors were a surprising find in two of the patients. The same loss in contiguous endometriosis, atypical in nature, was not evident in the distant lesions of endometriosis. This led the researchers to believe that it was, in fact, an early step during the transformation of endometriosis to cancer.
Dr. Huntsman also elaborates on the effectiveness of this study and hopes that the discovery would enable the physicians use it as a tool for screening endometriosis patients who have a high risk of developing ovarian cancer.
Another study by Siân Jones and his team of colleagues associated with Johns Hopkins Kimmel Cancer Cente, Baltimore, Maryland, also reported finding four different mutated genes in ovarian clear cell cancers. Of these, 2 of them had been previously known to scientists while ARID1A and PPP2R1A are new finds in the category. The results of this particular study had been published on the same day as that of the other one in Science.
Source: New England Journal of Medicine published online on September 8, 2010.
Science. 2010; published online on September 8, 2010
http://www.medscape.com/viewarticle/728251
