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|a dc
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|a Holst, Frederik
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|a Massachusetts Institute of Technology. Institute for Medical Engineering & Science
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|a Broad Institute of MIT and Harvard
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|a Harvard University-
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|a Gibson, William J
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|a Meyerson, Matthew L
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|a Beroukhim, Rameen
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|a Hoivik, Erling A.
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|a Taylor-Weiner, Amaro
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|a Schumacher, Steven E.
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|a Asmann, Yan W.
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|a Grossmann, Patrick
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|a Trovik, Jone
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|a Necela, Brian M.
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|a Thompson, E. Aubrey
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|a Salvesen, Helga B.
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|a Cherniack, Andrew D.
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|a Gibson, William J
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|a Beroukhim, Rameen
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|a Meyerson, Matthew L.
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|a Recurrent hormone-binding domain truncated ESR1 amplifications in primary endometrial cancers suggest their implication in hormone independent growth
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|b Nature Publiashing Group,
|c 2017-06-29T18:58:34Z.
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|z Get fulltext
|u http://hdl.handle.net/1721.1/110377
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|a The estrogen receptor alpha (ERα) is highly expressed in both endometrial and breast cancers, and represents the most prevalent therapeutic target in breast cancer. However, anti-estrogen therapy has not been shown to be effective in endometrial cancer. Recently it has been shown that hormone-binding domain alterations of ERα in breast cancer contribute to acquired resistance to anti-estrogen therapy. In analyses of genomic data from The Cancer Genome Atlas (TCGA), we observe that endometrial carcinomas manifest recurrent ESR1 gene amplifications that truncate the hormone-binding domain encoding region of ESR1 and are associated with reduced mRNA expression of exons encoding the hormone-binding domain. These findings support a role for hormone-binding alterations of ERα in primary endometrial cancer, with potentially important therapeutic implications.
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|a en_US
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|a Article
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|t Scientific Reports
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