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Epidermal Growth Factor Receptor-negative Tumors Are Predominantly Confined to the Subgroup of Estradiol Receptor-positive Human Primary Breast Cancers

Department of Experimental and Chemical Endocrinology [P. G. K., A. G-M., J. J. T. M. H., C. B. M. K., T. J. B.] and Department of Medicine [P. G. K., L. V. A. M. B.], Division of Endocrinology, University Hospital of Nijmegen, Nijmegen, The Netherlands

A total of 725 human primary breast tumor biopsy samples were analyzed for epidermal growth factor receptor (EGFR) content, using a multiple-point EGFR assay standardized in accordance with the recommendations of the European Organization for Research and Treatment of Cancer Receptor Study Group.

After the establishment of a lower cell membrane protein threshold of 0.2 mg of membrane protein per ml of assay buffer, the results of 27% (194 samples) of the EGFR determinations were excluded from the study because of insufficient assay membrane protein content. Of the remaining 531 breast tumor biopsy samples, 57% (302 samples) were shown to be EGFR positive by Scatchard analysis, with a median value of 40 fmol/mg of membrane protein.

Of the breast tumor biopsy samples, 72% (380 samples) were estrogen receptor (ER) positive, and 65% (344 samples) were progesterone receptor (PgR) positive. EGFR positivity was found in 46% (173 of 380) of ER-positive and in 85% (129 of 151) of ER-negative breast tumor biopsy samples (P < 0.0001), as well as in 49% (168 of 344) of PgR-positive and in 72% (134 of 186) of PgR-negative breast tumor biopsy samples (P < 0.0001). Mean EGFR levels in ER-positive breast tumor biopsy samples were lower than they were in ER-negative ones, 40 ± 31 (SD) against 72 ± 55 fmol/mg of membrane protein (P < 0.0001). Similarly, mean EGFR levels in PgR-positive breast tumor biopsy samples were lower than they were in PgR-negative ones, 41 ± 29 against 70 ± 56 fmol/mg of membrane protein (P < 0.0001). Both EGFR positivity and EGFR levels decreased with increasing steroid hormone receptor levels. A multivariate analysis showed only ER to be independently associated with EGFR.

¹ To whom requests for reprints should be addressed, at Department of Experimental and Chemical Endocrinology, University Hospital of Nijmegen, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands.

Received 3/11/91. Accepted 6/17/91.

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