Show simple item record

dc.contributor.authorHolst, Frederiken_US
dc.contributor.authorHøivik, Erling Andreen_US
dc.contributor.authorGibson, William J.en_US
dc.contributor.authorTaylor-Weiner, Amaroen_US
dc.contributor.authorSchumacher, Steven E.en_US
dc.contributor.authorAsmann, Yan W.en_US
dc.contributor.authorGrossmann, Patricken_US
dc.contributor.authorTrovik, Joneen_US
dc.contributor.authorNecela, Brian M.en_US
dc.contributor.authorThompson, E. Aubreyen_US
dc.contributor.authorMeyerson, Matthewen_US
dc.contributor.authorBeroukhim, Rameenen_US
dc.contributor.authorSalvesen, Helga Birgitteen_US
dc.contributor.authorCherniack, Andrew D.en_US
dc.PublishedScientific Reports 2016, 6:25521eng
dc.description.abstractThe 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.en_US
dc.publisherNature Publishing Groupeng
dc.rightsAttribution CC BYeng
dc.titleRecurrent hormone-binding domain truncated ESR1 amplifications in primary endometrial cancers suggest their implication in hormone independent growthen_US
dc.typePeer reviewed
dc.typeJournal article
dc.rights.holderCopyright 2016 The Author(s)

Files in this item


This item appears in the following Collection(s)

Show simple item record

Attribution CC BY
Except where otherwise noted, this item's license is described as Attribution CC BY