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Laboratory of Gynecologic Oncology, Division of Gynecologic Oncology, Department of Obstetrics, Gynecology, and Reproductive Biology [K. H. L., S. K., R. S. B., S. C. M.], and Department of Pathology [W. R. W.], Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, and Clinical Cancer Genetics, City of Hope National Medical Center, Duarte, California 91010 [J. N. W.]
Prior cytogenetic and restriction fragment length polymorphism studies have demonstrated that allelic deletion of chromosome 11p is common in human invasive epithelial ovarian tumors. To construct a highly detailed deletion map of chromosome 11p, we used 13 polymorphic microsatellite CA repeat primers to identify regions harboring potential tumor suppresser genes. Twenty-three of 48 samples (48%) of invasive epithelial ovarian cancer showed LOH involving at least one locus, consistent with prior studies. None of the five mucinous tumors showed allelic deletion at any of the 13 primers, suggesting that loss of heterozygosity at chromosome 11p may not be involved in the pathogenesis of mucinous ovarian cancer. Two separate minimally deleted regions were identified in nonmucinous ovarian cancer. The first is an 11-cM region on chromosome 11p15.515.3 that extends from D11S2071 to D11S988 and includes the HRAS locus. The second is a novel 4-cM region on 11p15.1, defined by marker D11S1310. Deletion of both regions at 11p15.515.3 and 11p15.1 is strongly associated with high grade nonmucinous epithelial ovarian cancer.
1 Supported by United States Public Health Service Grant R01CA63381 from the NIH, Department of Health and Human Services. J. N. W. was supported in part by NIH-Clinical Investigator Award 1 KO8 CAO1574.
2 To whom requests for reprints should be addressed, at Laboratory of Gynecologic Oncology, Brigham and Women's Hospital, 221 Longwood Ave., RF #472, Boston, MA 02115.
Received 10/22/96. Accepted 12/18/96.
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