Steroid Hormone Receptor Profile of Normal, Benign, and Malignant Female Breast Epithelium: An Immunohistochemical Analysis of 325 Biopsies

Abstract

: The steroid hormone receptor (SR) profile was determined for both the estrogen receptor (ER) and progesterone receptor (PR) in 55 fibroadenomas, 69 fibrocystic changes, 38 ordinary, and 14 atypical intraductal hyperplasias as well as 149 breast carcinomas obtained from 325 female patients by diagnostic surgical biopsy. Normal breast tissue adjacent to the lesions under study was simultaneously evaluated in 234 cases. SR were proven immunohistochemically in cryostat sections using an immunohistochemical assay with rat monoclonal antibodies against human ER or PR. The findings were scored and summarized into the phenotypes ER+PR+,ER−PR+, ER+PR− and ER−PR−. The ER+PR+ status was most often found in fibroadenomas (67%) and normal breast tissue (64%) as well as in fibrocystic changes (63%) and breast carcinomas (58%). ER−PR− was inversely rare in fibroadenomas (4%), normal breast tissue (15%), fibrocystic changes (23%), and breast carcinomas (29%). The simultaneous SR analysis in breast disease and its surrounding normal tissue showed in fibroadenomas in 90% and in fibrocystic changes in 80%, a ER/PR phenotype expression similar to adjacent normal tissue; whereas in breast carcinomas the SR status corresponded with the preexisting normal tissue only in 36%. The comparative SR analysis of normal and pathological breast tissue showed a gradually inverse biological correlation between the decrease of ER+PR+ and the increase of ER−PR− frequency from benign breast changes to noninvasive and invasive breast carcinomas. In benign breast epithelium, ER−PR+ might be regarded as low-risk phenotype, whereas ER+PR− could be estimated as high-risk phenotype in view of a later dedifferentiation and possible malignization. The more frequent discordance of SR expression between breast carcinomas and their adjacent normal breast tissue suggests that the neoplastic growth may become more and more independent from normal endocrine influences.