Abstract
It is fairly well accepted that the presence of estrogen receptor (ER) and progesterone receptor (PgR) identifies breast cancer patients with a lower risk of relapse and better overall survival. But patients with discordant receptors, the ER+/PgR- phenotype, are often intermediate in clinical response. We focused upon this group of patients and have identified a truncated ER which is abundant in some ER+/PgR- breast tumors and which inhibits the binding of wild-type ER to its cognate response element. This variant interferes in a dominant negative manner with wild-type ER function and may represent a mechanism for modulation of estrogen responsiveness.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Base Sequence
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Breast Neoplasms / physiopathology*
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DNA-Binding Proteins / genetics
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Exons
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Gene Expression Regulation, Neoplastic
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Genes, Dominant
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Humans
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Molecular Sequence Data
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Mutation
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Oligodeoxyribonucleotides / chemistry
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Polymerase Chain Reaction
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Receptors, Estrogen / genetics*
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Receptors, Estrogen / physiology
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Receptors, Progesterone / genetics
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Transcription Factors / genetics
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Transcription, Genetic / drug effects
Substances
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DNA-Binding Proteins
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Oligodeoxyribonucleotides
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Receptors, Estrogen
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Receptors, Progesterone
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Transcription Factors
Associated data
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GENBANK/S72766
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GENBANK/S72767
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GENBANK/S72768
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GENBANK/S72769
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GENBANK/S72771
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GENBANK/S72956
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GENBANK/S94172
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GENBANK/S94173
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GENBANK/X63098
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GENBANK/X68640