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American Journal of Pathology, Vol 145, 535-540, Copyright © 1994 by American Society for Investigative Pathology
REGULAR ARTICLES |
V Bhargava, DL Kell, M van de Rijn and RA Warnke
Department of Pathology, Stanford University School of Medicine, California.
The protein encoded by the Bcl-2 proto-oncogene has been shown to inhibit programmed cell death and has been primarily studied in hematolymphoid malignancies. Recent work ahs elucidated Bcl-2 expression in nonhematolymphoid malignancies of the lung, prostate, and nasopharynx. Studies of Bcl-2 expression in prostate carcinoma have suggested that its expression may be related to hormonal control. To determine its presence and possible significance in breast carcinoma, a malignancy in which therapy is influenced by hormone receptor status, we used a monoclonal antibody directed against the Bcl-2 gene product to examine Bcl-2 immunoreactivity in a series of paraffin-embedded primary breast tumors. Benign breast tissue showed Bcl-2 positivity in the basal layer and in superficial cells. Twenty-four of 41 (58%) carcinomas were Bcl-2 positive. Staining for Bcl-2 was equivocal in two cases. We identified a strong correlation between Bcl-2 expression and hormone receptor positivity as 23 of 24 (96%) cases that were Bcl-2 positive were estrogen receptor (ER) positive (P = 0.0001) and 21 of 24 (87.5%) were positive for progesterone receptor PR (P = 0.0001). Of 15 Bcl-2-negative cases, 14 (93%) were ER negative and all were PR negative. One case of mucinous carcinoma was ER positive and Bcl-2 negative. Grade 1 and 2 tumors (Scarff-Bloom-Richardson scale) were almost three times as likely to be Bcl-2 positive (90%) as grade 3 tumors (33%) (P = 0.0057). Bcl-2 reactivity appears to be more prevalent in well-differentiated tumors, suggesting that its presence may diminish with loss of differentiation, a hypothesis that is further supported by a subset of cases that were ER negative, Bcl-2 negative, and of poor histological grade. These may be tumors that do not require Bcl-2 inhibition of apoptosis and respond to hormonally independent proliferation factors. Our findings support the hypothesis that Bcl-2 expression may be related to hormonal regulation in breast carcinoma.
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