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An Exon 5 Deletion Variant of the Estrogen Receptor Frequently Coexpressed with Wild-Type Estrogen Receptor in Human Breast Cancer¹

Department of Oncology, University Hospital, S-221 85 Lund, Sweden [Q-X. Z., A. B.], and Department of Medicine/Medical Oncology, University of Texas Health Science Center, San Antonio, Texas 78284-7884 [S. A. W. F.]

Recent evidence suggests that the expression of estrogen receptor (ER) variants in breast cancer may interfere with wild-type (wt) ER function and be related to tumor progression and resistance to hormone treatment. One of these variants, ERE5, lacking that part of the hormone-binding domain encoded by exon 5, has previously been identified in breast tumors with the unusual estrogen receptor negative (ER–) and progesterone receptor positive (PgR+) phenotype and found to possess constitutive and hormone-independent transcriptional activity. Using a ribonuclease protection assay, we analyzed 27 breast tumors and 4 breast cell lines for the presence of this variant. We found the ERE5 variant to be expressed, not only in all of three ER–/PgR+ tumors but also in 19 of 20 ER+/PgR+ or ER+/PgR– tumors. Moreover, the variant was always coexpressed with and often in excess of wtER. ERE5 was also found in three breast cancer cell lines (MCF7, T47D, and ZR75-1), although to a lesser extent than wtER. A complete absence of both ERE5 and wtER was noted in four ER–/PgR– tumors and one normal breast cell line (HBL-100). Thus, our data suggest that the occurrence of ERE5 in breast cancer may represent a critical stage in tumor progression to autonomy.

¹ Supported by grants from the Swedish Cancer Society; the Gunnar, Arvid and Elisabeth Nilsson Cancer Foundation; the Thelma Zoega Foundation; and the CTR Foundation.

² To whom requests for reprints should be addressed.

Received 8/31/93. Accepted 11/10/93.

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