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Sci Rep. 2016 May 10;6:25521. doi: 10.1038/srep25521.

Recurrent hormone-binding domain truncated ESR1 amplifications in primary endometrial cancers suggest their implication in hormone independent growth.

Author information

1
Centre for Cancer Biomarkers, Department of Clinical Science, The University of Bergen, Norway.
2
KG Jebsen Center for Precision Medicine in Gynecologic Cancer, Department of Gynecology and Obstetrics, Haukeland University Hospital Bergen, Norway.
3
Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
4
Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA.
5
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
6
Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
7
Department of Health Sciences Research, Mayo Clinic Cancer Center, Jacksonville, Florida 32224, USA.
8
Department of Radiation Oncology, Dana-Farber Cancer Institute, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
9
Department of Biostatistics &Computational Biology, Dana-Farber Cancer Institute, Boston, MA, USA.
10
Department of Cancer Biology, Mayo Clinic Cancer Center, Jacksonville, Florida.
11
Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

Abstract

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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