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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TLDR
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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Pi3k/akt/mtor: вклад в формирование фенотипа опухоли, чувствительного к тамоксифену
TL;DR: The results of studies of the main components of the cascade as molecular markers of response to tamoxifen therapy in estrogen‑positive BC patients are presented and further study of the PI3K/Akt/mTOR crosstalk with various signaling pathways will contribute to both the understanding of carcino‑ genesis and the development of new molecular‑targeted anticancer drugs for the treatment of tamoxIFen‑ resistant breast tumors.
Book ChapterDOI
Role of Ancillary Tests in Breast Fine Needle Aspiration Biopsy Cytopathology
Francisco Beca,Fernando Schmitt +1 more
TL;DR: The complexity of the many challenges traditionally associated with the application of ancillary techniques to FNAB of the breast are elucidated to provide insights into some of the most cutting-edge and clinical useful application scenarios.
Posted ContentDOI
PAK4 regulates stemness and progression in endocrine resistant ER-positive metastatic breast cancer
Angélica Santiago-Gómez,Ilaria Dragoni,Roisin NicAmhlaoibh,Elisabeth Trivier,Verity Sabin,Bruno M Simões,Julia Margaret Wendy Gee,Andrew H. Sims,Sacha J Howell,Robert Clarke +9 more
TL;DR: It is established that PAK4 regulates stemness during disease progression and that its inhibition reverses endocrine resistance in ER+ breast cancers.
Book ChapterDOI
Molecular Classification of Breast Cancer
Maria Vidal,Laia Paré,Aleix Prat +2 more
TL;DR: The main molecular features of the intrinsic molecular subtypes of breast cancer and how the combination of standard clinical–pathological markers with the information provided by these molecular entities might help further understand the biological complexity of this disease, increase the efficacy of current and novel therapies, and ultimately improve outcomes for breast cancer patients are described.
Posted ContentDOI
Estrogen-independent molecular actions of mutant estrogen receptor alpha in endometrial cancer
Zannel Blanchard,Zannel Blanchard,Jeffery M. Vahrenkamp,Jeffery M. Vahrenkamp,Kristofer C. Berrett,Kristofer C. Berrett,Spencer Arnesen,Spencer Arnesen,Jason Gertz,Jason Gertz +9 more
TL;DR: Using a unique CRISPR/Cas9 strategy, the D538G mutation is introduced, a common endometrial cancer mutation that alters the ligand binding domain of ESR1, while epitope tagging the endogenous locus, and discovered estrogen-independent mutant E SR1 genomic binding that is significantly altered from wildtype ESR2.
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