Abstract
Endometrial carcinoma is the most common invasive malignancy of the female genital tract, and it exists as two different clinicopathologic forms: an estrogen-dependent, 'usual' type and an estrogen-independent 'special variant' type. Despite the frequency of endometrial cancer, little is known about the molecular genetic events that contribute to its pathogenesis. The accumulation of genetic alterations identified through the study of loss of heterozygosity (LOH), gene mutation, and gene activation in tumor DNA has been associated with the establishment and progression of a variety of human malignancies. A relatively low incidence of LOH has been reported in usual type endometrial cancers; however, special variant tumors have rarely been included in the reported studies. To understand the molecular events that contribute to both forms of endometrial cancer, 31 tumors have been surveyed for events of LOH on all chromosomes. The study groups included 18 tumors of the usual type and 13 special variant minors. Polymorphic loci were studied by Southern blot analysis and polymerase chain reaction (PCR) of microsatellite loci. Normal tissue in each case served as a control. Both frequency and patterns of LOH differed greatly between the two tumor types. Although LOH was frequently detected in the special variant tumors, it was rare in the usual type tumors. LOH was detected in only 8 of the 18 usual tumors, with chromosomes 17, 13, and 2 being the most frequently affected (22%, 20%, and 19%, respectively). In contrast, LOH was detected in all cases of special variant tumors, with chromosomes 17p, 14, and 12 showing the highest LOH (83%, 77%, and 40%, respectively). Two cases of microsatellite instability (MI) were detected among the usual type tumors. These findings suggest that the clinicopathologic phenotypes observed in these tumor types are likely caused by different tumorigenic pathways that reflect alterations of different cancer-controlling genes.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 607-612 |
| Number of pages | 6 |
| Journal | Human pathology |
| Volume | 28 |
| Issue number | 5 |
| DOIs | |
| State | Published - 1997 |
Bibliographical note
Funding Information:From the Department of Pathology and Laboratory Medicine, University of Kentucky, Lexington, KY. Accepted for publication September 23, 1996. Supported by grant no. IRG-77653 from the American Cancer Society (D.T.) and grant no. NIH-NCI CA60647 (M.P.). Presented in part at the 1994 and 1996 USCAP Annual Meetings in San Francisco, CA, and Washington, DC, respectively. Address correspondence and reprint requests to Denise Tritz, MD, Boyce and Byn..um Pathology Laboratories Inc, 2703 Clark Lane, Columbia, MO 65205. Copyright © 1997 by W.B. Saunders Company 0046-8177/97/2805-002155.00/0 LOH was frequently detected in the special variant armors, it was rare in the usual type tumors. LOH was detected in only 8 of the 18 usual tumors, with chromosomes 17, 13, and 2 being the most fre-quendy affected (22%, 20%, and 19%, respectively). In contrast, LOH was detected in all cases of special variant tumors, with chromosomes 17p, 14, and 12 showing the highest LOH (83%, 77%, and 40%, respectively). Two cases of microsatellite instability (MI) were de-teeted among the usual type tumors. These findings suggest that the clinlcopathologic phenotypes observed in these tumor types are likely caused by different tumorigenic pathways that reflect alterations of different cancer-controlling genes. HUM PATHOL 28:607--612. Copy-fight © 1997 by W.B. Satmders Company Key words: endometfial cancer, loss of heterozygosity, endometri-old adenocarcinoma, special variant carcinomas.
Keywords
- endometrial cancer
- endometrioid adenocarcinoma
- loss of heterozygosity
- special variant carcinomas
