The development of these drugs also may be important for other types of cancers that can involve deactivating the PTEN gene, Parsons said.
The study results were published online Dec. 9 in the journal Nature Genetics.
Parsons said the discovery of the PTEN deactivation "was kind of a real long-term detective story." For 10 years, researchers have been trying to understand how the mutation in the BRCA1 gene can cause breast cancer. Instead of using traditional gene-sequencing techniques, Parsons and his colleagues looked for physical breaks in the PTEN gene. "PTEN is actually physically broken in half, we estimate, in 30 to more than 50 percent of the BRCA1 tumors," he said.
Dr. Jeffrey Weitzel, an associate professor of medical oncology at the City of Hope Comprehensive Cancer Center in Duarte, Calif., said the study by Parsons' team "helps us understand what's under-appreciated in the complex nature of tumor changes."
Andrew Godwin, director of the clinical molecular genetics laboratory at the Fox Chase Cancer Center in Philadelphia, added: "As we move towards personalized health care [and] medicine, identifying the cadre of genetic defects in a given breast tumor will likely influence how that patient is ultimately treated."
For more on breast cancer, visit the U.S. National Cancer Institute.
SOURCES: Andrew Godwin, Ph.D., director, Clinical Molecular Genetics Laboratory and the Biosample Repository, Fox Chase Cancer Center, Philadelphia; Ramon Parsons, M.D., Ph.D., director of the Breast Cancer Program of the Herbert Irving Comprehensive Cancer Center of Columbia University Medical Center and New York-Presbyterian Hospital, and professor of medicine and path
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