16 September 2010

Researchers Identify Genes Tied to Deadliest Ovarian Cancers

Aumenta dimensioni testoDiminuisci dimensioni testo
Scientists at the Johns Hopkins Kimmel Cancer Center have identified two genes whose mutations appear to be linked to ovarian clear cell carcinoma, one of the most aggressive forms of ovarian cancer. Clear cell carcinoma is generally resistant to standard therapy.
In an article published online in the September 8 issue of Science Express, the researchers report that they found an average of 20 mutated genes per each ovarian clear cell cancer studied. Two of the genes were more commonly mutated among the samples: ARID1A, a gene whose product normally suppresses tumors, and PPP2R1A, an oncogene that, when altered, helps turn normal cells into tumor cells. ARID1A mutations were identified in more than half of the tumors studied, and, according to Siân Jones, Ph.D., research associate at the Johns Hopkins Kimmel Cancer Center, “this gene may play a significant role in this type of cancer.”

The researchers say that ARID1A and PPP2R1A had not previously been linked to ovarian cancer, and “they may provide opportunities for developing new biomarkers and therapies that target those genes,” says Nickolas Papadopoulos, Ph.D., an associate professor of oncology and director of Translational Genetics at the Ludwig Center for Cancer Genetics & Therapeutics at the Johns Hopkins Kimmel Cancer Center.

For the study, the scientists evaluated mutations in 18,000 protein-encoding genes in ovarian clear cell tumors from eight patients at Johns Hopkins and from institutions in Taiwan and Japan. They purified the cancer cells, and analyzed genes from those cells and from normal cells obtained from the blood or uninvolved tissues of the same patients.

Researchers identified 268 mutations in 253 genes among the eight tumors, with an average of 20 mutations per tumor.

(insciences.org)

Read more
youris.com provides its content to all media free of charge. We would appreciate if you could acknowledge youris.com as the source of the content.