Activating ESR1 mutations in hormone-resistant metastatic breast cancer
Dan R. Robinson,Yi-Mi Wu,Pankaj Vats,Fengyun Su,Robert J. Lonigro,Xuhong Cao,Shanker Kalyana-Sundaram,Rui Wang,Yu Ning,Lynda Hodges,Amy Gursky,Javed Siddiqui,Scott A. Tomlins,Sameek Roychowdhury,Kenneth J. Pienta,Scott Y. H. Kim,J. Scott Roberts,James M. Rae,Catherine Van Poznak,Daniel F. Hayes,Rashmi Chugh,Lakshmi P. Kunju,Moshe Talpaz,Anne F. Schott,Arul M. Chinnaiyan +24 more
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Five new LBD-localized ESR1 mutations identified here were shown to result in constitutive activity and continued responsiveness to anti-estrogen therapies in vitro, suggesting that activating mutations in E SR1 are a key mechanism in acquired endocrine resistance in breast cancer therapy.Abstract:
Arul Chinnaiyan and colleagues report the results of prospective clinical sequencing of 11 estrogen receptor–positive metastatic breast cancers. They identify ESR1 mutations affecting the ligand-binding domain in six hormone-resistant metastatic breast cancers and show that the mutant estrogen receptors are constitutively active and continue to be responsive to anti-estrogen therapies in vitro. Breast cancer is the most prevalent cancer in women, and over two-thirds of cases express estrogen receptor-α (ER-α, encoded by ESR1). Through a prospective clinical sequencing program for advanced cancers, we enrolled 11 patients with ER-positive metastatic breast cancer. Whole-exome and transcriptome analysis showed that six cases harbored mutations of ESR1 affecting its ligand-binding domain (LBD), all of whom had been treated with anti-estrogens and estrogen deprivation therapies. A survey of The Cancer Genome Atlas (TCGA) identified four endometrial cancers with similar mutations of ESR1. The five new LBD-localized ESR1 mutations identified here (encoding p.Leu536Gln, p.Tyr537Ser, p.Tyr537Cys, p.Tyr537Asn and p.Asp538Gly) were shown to result in constitutive activity and continued responsiveness to anti-estrogen therapies in vitro. Taken together, these studies suggest that activating mutations in ESR1 are a key mechanism in acquired endocrine resistance in breast cancer therapy.read more
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SETER/PR: a robust 18-gene predictor for sensitivity to endocrine therapy for metastatic breast cancer.
Bruno Valentin Sinn,Bruno Valentin Sinn,Chunxiao Fu,Rosanna Lau,Jennifer K. Litton,Tsung-Heng Tsai,Rashmi Krishna Murthy,Alda L. Tam,Eleni Andreopoulou,Eleni Andreopoulou,Yun Gong,Ravi Murthy,Rebekah Gould,Ya Zhang,Tari A. King,Agnes Viale,Victor P. Andrade,Dilip Giri,Roberto Salgado,Ioanna Laïos,Christos Sotiriou,Esmeralda Celia Marginean,Danielle N. Kwiatkowski,Rachel M. Layman,Daniel J. Booser,Christos Hatzis,Vicente Valero,W. Fraser Symmans +27 more
TL;DR: Elevated SETER/PR was associated with prolonged sensitivity to endocrine therapy in patients with metastatic HR+/HER2− breast cancer, especially in the absence of mutated ESR1 transcript.
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Comprehensive Genomic Analysis Reveals that the Pioneering Function of FOXA1 Is Independent of Hormonal Signaling.
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The importance of molecular markers for diagnosis and selection of targeted treatments in patients with cancer
TL;DR: This review focuses on three tumour types: breast, lung and colorectal cancers, and provides a background to the disease along with an overview of the current standard therapies and then focuses on the relevant targeted therapies and the pathways they inhibit.
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