Previous studies indicate that activation of the epidermal growth factor receptor (EGFR) can stimulate the growth of cancer cells. Mutations within the tyrosine kinase (TK) portion of this receptor may give cancer cells a growth advantage but at the same time make them more susceptible to drugs, like gefitinib, which inhibit growth. Gefitinib does not appear to be effective in women whose cancer does not have a mutation in the TK portion of EGFR.
"Researchers continue to study how best to incorporate EGFR-inhibiting drugs into therapy for ovarian cancer, but that requires a cost-effective way to screen patients to identify various mutations," said lead researcher Russell Schilder, M.D., a medical oncologist at Fox Chase. "In regard to ovarian cancer, there are 25,000 cases diagnosed annually. Someday, we'll be able to sequence key genes in ovarian tumors to identify the women who would be responsive to gefitinib or other targeted therapies."
The Fox Chase translational research team headed by Schilder and Andrew K. Godwin, Ph.D., director of Fox Chase's Clinical Molecular Genetics Laboratory, where the mutation studies were performed, was spurred by recent studies that indicated the same mutations appear to identify lung cancer patients who respond well to gefitinib therapy. Gefitinib has been used as a single agent to treat patients with recurrent non-small-cell lung cancer (NSCLC). Schilder and Godwin have replicated this finding retrospectively in ovarian cancer samples. "This was the first report that has documented mutations in the EGFR in ovarian cancer," Schilder said.