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Estrogen receptor mutagenesis and hormone resistance
Author(s) -
Fuqua Suzanne A. W.
Publication year - 1994
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(19940801)74:3+<1026::aid-cncr2820741509>3.0.co;2-k
Subject(s) - estrogen receptor , tamoxifen , receptor , transfection , estrogen related receptor alpha , exon , estrogen receptor alpha , cancer research , estrogen related receptor gamma , endocrinology , biology , estrogen receptor beta , medicine , genetics , gene , cancer , breast cancer
The authors have detected a truncated receptor that is lacking the majority of the hormone‐binding domain because of the deletion of exon 5. This variant acts as a dominant‐positive receptor in the absence of hormones. The exon 5 estrogen receptor (ER) variant, although originally identified in ER‐negative, progesterone receptor‐positive tumors, now has been found to be coexpressed at variable levels with the wild‐type receptor in a large number of ER‐positive tumors. Therefore, to establish the significance of its coexpression with the wild‐type receptor, the authors transfected the variant into ER‐positive MCF‐7 cells. MCF‐7 transfected cells that now express equivalent levels of the variant as compared with the wild‐type receptor are resistant to the growth‐inhibitory effects of tamoxifen. The authors hypothesize that the exon 5 ER deletion variant may be involved in clinical tamoxifen resistance and hormone independence.