PI3K pathway regulates ER-dependent transcription in breast cancer through the epigenetic regulator KMT2D

Author:

Toska Eneda1ORCID,Osmanbeyoglu Hatice U.2,Castel Pau13ORCID,Chan Carmen1ORCID,Hendrickson Ronald C.4ORCID,Elkabets Moshe15ORCID,Dickler Maura N.6,Scaltriti Maurizio17ORCID,Leslie Christina S.2ORCID,Armstrong Scott A.89ORCID,Baselga José16ORCID

Affiliation:

1. Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 20, New York, NY 10065, USA.

2. Computational Biology Program, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 460, New York, NY 10065, USA.

3. Helen Diller Family Comprehensive Cancer Center, University of California–San Francisco, 1450 3rd Street, San Francisco, CA 94158, USA.

4. Microchemistry and Proteomics Core Laboratory, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.

5. The Shraga Segal Department of Microbiology, Immunology and Genetics, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel.

6. Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.

7. Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.

8. Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.

9. Department of Pediatric Oncology, Dana-Farber Cancer Institute, 450 Brookline Avenue, Boston, MA 02215, USA.

Abstract

Tumor cells develop resistance to a drug used to treat breast cancer through a chromatin remodeling mechanism.

Funder

Breast Cancer Research Foundation

Geoffrey Beene Cancer Research Center

NIH

NCI

Terri Brodeur Breast Cancer Foundation

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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