Activated FGFR2 as a Viable Therapeutic Target in a Subset of Ovarian Cancers
Abstract
Ovarian cancer is the leading cause of death from gynecologic malignancies in the Western world. Fibroblast growth factor receptor (FGFR) signaling has been implicated to play a role in ovarian tumorigenesis. Given our recent report of activating mutations in FGFR2 in endometrioid endometrial tumors and the similarities in the molecular genetics of ovarian and endometrial cancer, we hypothesized that activating FGFR2 mutations may also occur in a subset of ovarian tumors, particularly in the endometrioid subtype. Methods: Six exons of FGFR2 were sequenced in 120 ovarian tumors representing the various histotypes of ovarian cancer. Results: Mutation of FGFR2 was detected at low frequency in endometrioid (1/46, 2.2%) and serous (1/41, 2.4%) ovarian cancer. No mutations were detected in clear cell, mucinous, or mixed histology tumors or in the ovarian cancer cell lines tested. Functional characterization of the FGFR2 mutations confirmed that the mutations detected in ovarian cancer result in receptor activation. Conclusions: Despite the low incidence of FGFR2 mutations in ovarian cancer, the development and validation of anti-FGFR agents in other cancer types may allow for the future use of these agents in the small subset of ovarian cancer patients whose tumors possess activating FGFR2 mutations.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2009
- Accession Number
- ADA511226
Entities
People
- Pamela Pollack
Organizations
- Translational Genomics Research Institute