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Oestrogen receptors alpha and beta differ in normal human breast and breast carcinomas
Author(s) -
Shaw Jacqueline A,
Udokang Kufre,
Mosquera JuanMiguel,
Chauhan Hina,
Jones J Louise,
Walker Rosemary A
Publication year - 2002
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1230
Subject(s) - myoepithelial cell , breast cancer , estrogen receptor alpha , estrogen receptor , immunohistochemistry , progesterone receptor , medicine , estrogen receptor beta , mammary gland , estrogen , endocrinology , receptor , carcinogenesis , biology , cancer research , cancer
The identification of a second oestrogen receptor, oestrogen receptor (ER) β, has led to a need to assess the relative importance of the classical ERα and ERβ in human breast and breast carcinomas. ERα and ERβ mRNA was assessed in 61 carcinomas, 8 benign breast lesions, and 30 samples of normal breast using reverse transcriptase (RT)‐nested polymerase chain reaction (PCR). Immunohistochemical analysis of ERα and ERβ was performed in 62 carcinomas, the 38 non‐malignant breast tissues, and 32 normal breast samples with menstrual cycle data. ERα mRNA was detected in 92% of breast cancers, with ERβ mRNA (wild‐type and/or variant form) in 85%; 72% had ERα protein, 62% progesterone receptor (PgR), and 32% ERβ. ERα protein had a strong correlation with grade; ERβ did not, although it was present in three of four grade I carcinomas and in special types. There was no correlation between the presence of ERα and ERβ protein. In non‐malignant breast, similar expression of ERα and β was observed, apart from expression of ERβ in stromal cells and myoepithelium, the latter being confirmed by RT‐PCR and western blotting. There were differences in ERα in relation to the menstrual cycle but not PgR or ERβ. The findings indicate a need to understand the role and regulation of ERβ in normal breast and the reason for its down‐regulation in mammary carcinogenesis. Copyright © 2002 John Wiley & Sons, Ltd.