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The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 3 1200-1205
Copyright © 2000 by The Endocrine Society

Original Studies

Estrogen Receptor Isoform Gene Expression in Ovarian Stromal and Epithelial Tumors1

Simon Chu, Pam Mamers, Henry G. Burger and Peter J. Fuller2

Prince Henry’s Institute of Medical Research and the Monash University Department of Obstetrics and Gynecology, Monash Medical Center, Clayton, Victoria 3168, Australia

Address all correspondence and requests for reprints to: Dr. Peter J. Fuller, Prince Henry’s Institute of Medical Research, P.O. Box 5152, Clayton, Victoria 3168, Australia. E-mail: peter.fuller{at}med.monash.edu.au

The factors involved in the pathogenesis of ovarian cancers remain unclear, and the response of these tumors to hormonal therapy is limited. The identification of a second estrogen receptor gene (ERß), expressed predominantly in ovarian granulosa cells, led us to explore its possible role in ovarian cancer, particularly in granulosa cell tumors (GCT). Several isoforms of ERß have been identified. We sought to define the patterns of both ER{alpha} and ERß gene expression in a panel of ovarian tumors consisting of GCT and serous and mucinous cystadenocarcinomas as well as in normal ovary. Expression was determined by RT-PCR using gene- and isoform-specific primers and probes combined with Southern blot analysis of the PCR products. Widespread expression of ER{alpha} was observed in all tumor types, but at relatively low levels. ERß is expressed predominantly in GCT, with lower levels in mucinous tumors and very low levels in serous tumors. The ERß2 splice variant previously reported in rodents was not observed. Only very low levels of the exon 5, exon 6, and exon 5/6 deletion variants were detected. The C-terminal truncation variant ERßcx, however, exhibited widespread expression across all the tumor types. As ERßcx has been shown to be a ligand-independent antagonist of ER{alpha} action, the relative ratios of ERßcx, ER{alpha}, and ERß may influence the response of a tumor to antiestrogen therapy.




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