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[Cancer Research 52, 2597-2602, May 1, 1992]
© 1992 American Association for Cancer Research

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c-myc, c-erbB-2, and Ki-67 Expression in Normal Breast Tissue and in Invasive and Noninvasive Breast Carcinoma1

Zlatko P. Pavelic2, Ljiljana Pavelic, Elyse E. Lower, Markus Gapany, Sabina Gapany, Edward A. Barker and Harvey D. Preisler

Departments of Otolaryngology-Head and Neck Surgery [Z. P. P., L. P., M. G., S. G.] and Internal Medicine [E. E. L., H. D. P.], College of Medicine, University of Cincinnati, Cincinnati, Ohio 45267-0528, and Molecular Oncology, Inc., Gaithersburg, Maryland 20878 [E. A. B.]

c-myc, c-erbB-2, and Ki-67 expression was examined by immunohistochemistry in 11 normal breast tissues and 42 invasive and 14 noninvasive breast carcinomas. The c-myc product was detected in all breast carcinoma specimens and in 7 of 11 normal breast tissues. Invasive tumors stained more frequently with the anti-myc monoclonal antibody than did noninvasive tumors, while the level of expression in normal breast tissue was much less than that in breast cancer. Membrane staining of the c-erbB-2 protein was demonstrated in 29% (4 of 14) of noninvasive ductal carcinomas and in 45% (19 of 42) of invasive breast carcinomas. None of the 11 normal breast tissue samples was positive. The mean value of Ki-67-positive cells was 0.91 ± 0.31% for normal breast tissue, 4.57 ± 1.36% for noninvasive ductal carcinoma, and 12.76 ± 2.18% for invasive breast cancer. In 42 invasive breast carcinomas, the expression of c-myc, c-erbB-2, and Ki-67 proliferation marker were compared with lymph node status, estrogen receptor status, progesterone receptor status, and age of patients at diagnosis. c-erbB-2 overexpression and Ki-67 overexpression were identified as the only factors associated with lymph node status. We concluded that they might be additional prognostic factors for breast carcinoma.

1 This work was supported in part by a grant from NIH (CA 41285), a grant from the American Cancer Society, and a University Research Council grant from the University of Cincinnati. Part of this paper was presented at the 1990 Annual Meeting of the American Association for Cancer Research, Washington, DC.

2 To whom requests for reprints should be addressed, at the Department of Otolaryngology-Head and Neck Surgery, College of Medicine, University of Cincinnati, 231 Bethesda Avenue, Cincinnati, OH 45267-0528.

Received 8/ 7/90. Accepted 2/26/92.




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Copyright © 1992 by the American Association for Cancer Research.