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Frequent Loss of Heterozygosity on Chromosomes 6q, 11, and 17 in Human Ovarian Carcinomas¹

Department of Medical Oncology [J. H. L., J. J. K., D. M. W.], Department of Gynecology [J. T. W.], and Department of Clinical Immunology and Biological Therapy [M. B.], The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030

Recently, tumor-specific allele loss has been shown to be an important characteristic of some tumors. When such loss includes one or more growth-regulatory genes, it may allow the expression of tumorigenicity. Using Southern blots, we analyzed normal and tumor DNA samples from 19 ovarian cancer patients, using a series of polymorphic DNA probes that map to a variety of chromosomal loci. Of 14 informative cases, tumor-specific allelic loss was observed in nine (64%) at the estrogen receptor (ESR) gene locus on chromosome 6q. On chromosome 17p at the D17S28 and D17S30 loci, allelic losses were also detected in 6 of 8 (75%) and 9 of 14 (64%) cases, respectively. Allelic loss at the HRAS1 gene locus on chromosome 11p occurred in 5 of 11 (46%) informative cases. The relatively high incidence of these allelic losses observed on chromosome 6q represents the first implication by molecular genetic analysis of this chromosomal region in a human malignancy, and it thus appears to be a genetic change specific to ovarian carcinoma. DNA sequence losses on 11p and 17p, also reported for other cancers, may reflect the presence of tumor- or growth-suppressor genes on these chromosomes that are important in the genesis of many tumor types, including ovarian malignancies.

¹ Supported by an Institutional Research Grant, The University of Texas M. D. Anderson Cancer Center, Houston, TX, and the Bessie Frisch Memorial Fund.

² To whom requests for reprints should be addressed, at Molecular Analysis Incorporated, 8000 El Rio, Houston, TX 77054.

Received 6/ 9/89. Revised 12/21/89.

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