Researchers at the Translational Genomics Research Institute announced the discovery of previously unrecognized alterations in a gene called FGFR2 in a subset of endometrial cancers, the most common gynecologic cancer in the United States. The mutations in FGFR2 result in uncontrolled cell division, a hallmark of cancer. The findings, reported by TGen and research colleagues at Washington University School of Medicine in St. Louis, the Wellcome Trust Sanger Institute, which is part of Cambridge University, and New York University School of Medicine, could accelerate the development of new treatments for endometrial cancer because there are drugs already in clinical trials that inhibit FGFR2 function. The study appears in the May 21, 2007 online version of the journal Oncogene.
Nearly 40,000 women are diagnosed with endometrial cancer each year, making it the fourth most common cancer found in women, following breast cancer, lung cancer and colon cancer. Endometrial cancer usually begins in the lining of the uterus and is most commonly found in women between the ages of 60 and 70. If discovered early, this slow-growing cancer can be successfully treated by surgical removal of the uterus. However, about 7,000 women die each year from the more aggressive form of endometrial cancer.
Researchers at TGen used the latest genome-scanning technology to sequence 187 endometrial tumor samples. The research team identified mutations in FGFR2 in 16% of tumors that represented a specific subset of endometrial cancer. The other types of endometrial cancer did not have these mutations. The FGFR2 gene encodes a protein that plays a critical role in cell growth. In patients with FGFR2 mutations, the tumors were caused by the receptor for this protein being permanently stuck in the “on” position.