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Laboratory of Gynecologic Oncology, Department of Obstetrics, Gynecology, and Reproductive Biology, Brigham and Women's Hospital [S. C-H. M., R. C. K., P. M. F., M. G. M., R. S. B., S-W. T.]; Division of Gynecologic Oncology, Dana-Farber Cancer Institute [R. C. K., M. G. M., R. S. B., S-W. T.]; Division of Women's and Perinatal Pathology, Brigham and Women's Hospital [W. R. W.]; and Department of Pathology, Massachusetts General Hospital, Harvard Medical School [D. A. B.], Boston, Massachusetts 02115
The mutation of K-ras protooncogene was examined in 44 cases of borderline ovarian epithelial tumors and 18 cases of invasive ovarian carcinomas. In borderline tumors, K-ras mutations are a common feature, having been found in 21 of 44 cases (48%). Twenty of the 21 mutations were identified at codon 12, and one was identified at codon 13. A detailed analysis of the mutation pattern of K-ras revealed a close association with the histological cell types of the tumor. Mutation of K-ras was detected at a higher frequency in mucinous borderline tumor (identified in 12 of 19 cases) compared to serous borderline tumor (identified in 9 of 25 cases). K-ras mutation was also detected in invasive mucinous and serous ovarian carcinomas, hence supporting the notion that borderline ovarian tumors may represent a pathological continuum between benign and frankly invasive diseases.
1 Supported in part by the William Graves Ovarian Research Fund, Boston, MA, and by a research grant from Centocor, Inc., Malvern, PA.
2 To whom requests for reprints should be addressed, at Room 210, Seeley G. Mudd Building, 250 Longwood Avenue, Boston, MA 02115.
Received 1/11/93. Accepted 2/18/93.
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