Alterations in PTEN and ESR1 promote clinical resistance to alpelisib plus aromatase inhibitors
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M. Berger | S. Chandarlapaty | C. Hudis | J. Reis-Filho | L. Norton | R. Shen | E. Brogi | D. Solit | M. Robson | M. Lacouture | A. Covey | P. Razavi | H. Won | David N. Brown | M. Scaltriti | M. Moynahan | K. Jhaveri | J. Odegaard | S. Modi | and Singh | M. Dickler | Bob T. Li | S. Patil | R. Lanman | Weiyi Toy | E. Comen | P. Shah | N. Vasan | P. Selenica | B. A. Caravella | R. Nagy | S. Zamora | A. Cowan | R. Shen
[1] David R. Jones,et al. High-intensity sequencing reveals the sources of plasma circulating cell-free DNA variants , 2019, Nature Medicine.
[2] R. Kimmig,et al. Targeted deep sequencing revealed variants in cell-free DNA of hormone receptor-positive metastatic breast cancer patients , 2019, Cellular and Molecular Life Sciences.
[3] H. Rugo,et al. Alpelisib for PIK3CA‐Mutated, Hormone Receptor–Positive Advanced Breast Cancer , 2019, The New England journal of medicine.
[4] P. Fasching,et al. A Phase II Randomized Study of Neoadjuvant Letrozole Plus Alpelisib for Hormone Receptor-Positive, Human Epidermal Growth Factor Receptor 2-Negative Breast Cancer (NEO-ORB) , 2019, Clinical Cancer Research.
[5] J. Baselga,et al. Alpelisib Plus Fulvestrant in PIK3CA-Altered and PIK3CA-Wild-Type Estrogen Receptor–Positive Advanced Breast Cancer: A Phase 1b Clinical Trial , 2019, JAMA oncology.
[6] B. Taylor,et al. The Genomic Landscape of Endocrine-Resistant Advanced Breast Cancers. , 2018, Cancer cell.
[7] A. Bardelli,et al. Radiologic and Genomic Evolution of Individual Metastases during HER2 Blockade in Colorectal Cancer. , 2018, Cancer cell.
[8] J. Baselga,et al. Phase III study of taselisib (GDC-0032) + fulvestrant (FULV) v FULV in patients (pts) with estrogen receptor (ER)-positive, PIK3CA-mutant (MUT), locally advanced or metastatic breast cancer (MBC): Primary analysis from SANDPIPER. , 2018, Journal of Clinical Oncology.
[9] C. Paweletz,et al. Validation of a Plasma-Based Comprehensive Cancer Genotyping Assay Utilizing Orthogonal Tissue- and Plasma-Based Methodologies , 2018, Clinical Cancer Research.
[10] T. Pons,et al. Exome Sequencing of Plasma DNA Portrays the Mutation Landscape of Colorectal Cancer and Discovers Mutated VEGFR2 Receptors as Modulators of Antiangiogenic Therapies , 2018, Clinical Cancer Research.
[11] Dejan Juric,et al. Phosphatidylinositol 3-Kinase α-Selective Inhibition With Alpelisib (BYL719) in PIK3CA-Altered Solid Tumors: Results From the First-in-Human Study. , 2018, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[12] S. Mortimer,et al. The Landscape of Actionable Genomic Alterations in Cell-Free Circulating Tumor DNA from 21,807 Advanced Cancer Patients , 2017, Clinical Cancer Research.
[13] O. Delattre,et al. Whole-Exome Sequencing of Cell-Free DNA Reveals Temporo-spatial Heterogeneity and Identifies Treatment-Resistant Clones in Neuroblastoma , 2017, Clinical Cancer Research.
[14] Norikazu Masuda,et al. Buparlisib plus fulvestrant versus placebo plus fulvestrant in postmenopausal, hormone receptor-positive, HER2-negative, advanced breast cancer (BELLE-2): a randomised, double-blind, placebo-controlled, phase 3 trial. , 2017, The Lancet. Oncology.
[15] Donavan T. Cheng,et al. Comprehensive detection of germline variants by MSK-IMPACT, a clinical diagnostic platform for solid tumor molecular oncology and concurrent cancer predisposition testing , 2017, BMC Medical Genomics.
[16] Moriah H Nissan,et al. OncoKB: A Precision Oncology Knowledge Base. , 2017, JCO precision oncology.
[17] R. Peach,et al. Results From the First‐in‐Human Study With Ozanimod, a Novel, Selective Sphingosine‐1‐Phosphate Receptor Modulator , 2017, Journal of clinical pharmacology.
[18] Donavan T. Cheng,et al. Mutational Landscape of Metastatic Cancer Revealed from Prospective Clinical Sequencing of 10,000 Patients , 2017, Nature Medicine.
[19] A. Viale,et al. Genetic Heterogeneity in Therapy-Naïve Synchronous Primary Breast Cancers and Their Metastases , 2017, Clinical Cancer Research.
[20] Maurizio Scaltriti,et al. PI3K pathway regulates ER-dependent transcription in breast cancer through the epigenetic regulator KMT2D , 2017, Science.
[21] J. Baselga,et al. Phase I Dose-Escalation Study of Taselisib, an Oral PI3K Inhibitor, in Patients with Advanced Solid Tumors. , 2017, Cancer discovery.
[22] D. Fabbro,et al. Deconvolution of Buparlisib's mechanism of action defines specific PI3K and tubulin inhibitors for therapeutic intervention , 2017, Nature Communications.
[23] G. Hortobagyi,et al. Prevalence of ESR1 Mutations in Cell-Free DNA and Outcomes in Metastatic Breast Cancer: A Secondary Analysis of the BOLERO-2 Clinical Trial. , 2016, JAMA oncology.
[24] R. Motzer,et al. A Phase Ib Study of BEZ235, a Dual Inhibitor of Phosphatidylinositol 3-Kinase (PI3K) and Mammalian Target of Rapamycin (mTOR), in Patients With Advanced Renal Cell Carcinoma , 2016, The oncologist.
[25] V. Seshan,et al. FACETS: allele-specific copy number and clonal heterogeneity analysis tool for high-throughput DNA sequencing , 2016, Nucleic acids research.
[26] G. Hampton,et al. Heterogeneity and clinical significance of ESR1 mutations in ER-positive metastatic breast cancer patients receiving fulvestrant , 2016, Nature Communications.
[27] E. Winer,et al. A Phase Ib Study of Alpelisib (BYL719), a PI3Kα-Specific Inhibitor, with Letrozole in ER+/HER2− Metastatic Breast Cancer , 2016, Clinical Cancer Research.
[28] B. Taylor,et al. deconstructSigs: delineating mutational processes in single tumors distinguishes DNA repair deficiencies and patterns of carcinoma evolution , 2016, Genome Biology.
[29] M. Dowsett,et al. Analysis of ESR1 mutation in circulating tumor DNA demonstrates evolution during therapy for metastatic breast cancer , 2015, Science Translational Medicine.
[30] Carlos Caldas,et al. Multifocal clonal evolution characterized using circulating tumour DNA in a case of metastatic breast cancer , 2015, Nature Communications.
[31] B. Kermani,et al. Analytical and Clinical Validation of a Digital Sequencing Panel for Quantitative, Highly Accurate Evaluation of Cell-Free Circulating Tumor DNA , 2015, PloS one.
[32] N. Tunariu,et al. Serial Next-Generation Sequencing of Circulating Cell-Free DNA Evaluating Tumor Clone Response To Molecularly Targeted Drug Administration , 2015, Clinical Cancer Research.
[33] Andrew Menzies,et al. Subclonal diversification of primary breast cancer revealed by multiregion sequencing , 2015, Nature Medicine.
[34] J. Reis-Filho,et al. Intra-tumor genetic heterogeneity and alternative driver genetic alterations in breast cancers with heterogeneous HER2 gene amplification , 2015, Genome Biology.
[35] Donavan T. Cheng,et al. Memorial Sloan Kettering-Integrated Mutation Profiling of Actionable Cancer Targets (MSK-IMPACT): A Hybridization Capture-Based Next-Generation Sequencing Clinical Assay for Solid Tumor Molecular Oncology. , 2015, The Journal of molecular diagnostics : JMD.
[36] M. Ellis,et al. Mechanisms of aromatase inhibitor resistance , 2015, Nature Reviews Cancer.
[37] Michael G. Kharas,et al. PI3K inhibition results in enhanced estrogen receptor function and dependence in hormone receptor–positive breast cancer , 2015, Science Translational Medicine.
[38] J. Ware,et al. First-in-Human Phase I Study of Pictilisib (GDC-0941), a Potent Pan–Class I Phosphatidylinositol-3-Kinase (PI3K) Inhibitor, in Patients with Advanced Solid Tumors , 2014, Clinical Cancer Research.
[39] Obi L. Griffith,et al. Convergent loss of PTEN leads to clinical resistance to a PI3Kα inhibitor , 2014, Nature.
[40] M. Berger,et al. Capturing intra-tumor genetic heterogeneity by de novo mutation profiling of circulating cell-free tumor DNA: a proof-of-principle. , 2014, Annals of oncology : official journal of the European Society for Medical Oncology.
[41] S. Chandarlapaty,et al. Rapid induction of apoptosis by PI3K inhibitors is dependent upon their transient inhibition of RAS-ERK signaling. , 2014, Cancer discovery.
[42] Ash A. Alizadeh,et al. An ultrasensitive method for quantitating circulating tumor DNA with broad patient coverage , 2013, Nature Medicine.
[43] David Chen,et al. ESR1 ligand binding domain mutations in hormone-resistant breast cancer , 2013, Nature Genetics.
[44] C. Arteaga,et al. Autocrine IGF-I/insulin receptor axis compensates for inhibition of AKT in ER-positive breast cancer cells with resistance to estrogen deprivation , 2013, Breast Cancer Research.
[45] A. Wolff,et al. The phosphoinositide-3-kinase-Akt-mTOR pathway as a therapeutic target in breast cancer. , 2013, Journal of the National Comprehensive Cancer Network : JNCCN.
[46] N. Rosenfeld,et al. Non-invasive analysis of acquired resistance to cancer therapy by sequencing of plasma DNA , 2013, Nature.
[47] Carlos Caldas,et al. Analysis of circulating tumor DNA to monitor metastatic breast cancer. , 2013, The New England journal of medicine.
[48] Steven J. M. Jones,et al. Comprehensive molecular portraits of human breast tumors , 2012, Nature.
[49] A. McKenna,et al. Absolute quantification of somatic DNA alterations in human cancer , 2012, Nature Biotechnology.
[50] Jordi Rodon,et al. Phase I, dose-escalation study of BKM120, an oral pan-Class I PI3K inhibitor, in patients with advanced solid tumors. , 2012, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[51] Víctor J Cid,et al. A comprehensive functional analysis of PTEN mutations: implications in tumor- and autism-related syndromes. , 2011, Human molecular genetics.
[52] Alice T. Loo,et al. PTEN-deficient cancers depend on PIK3CB , 2008, Proceedings of the National Academy of Sciences.
[53] M. Jeschke. Faculty Opinions recommendation of Essential roles of PI(3)K-p110beta in cell growth, metabolism and tumorigenesis. , 2008 .
[54] M. Loda,et al. Essential roles of PI(3)K–p110β in cell growth, metabolism and tumorigenesis , 2008, Nature.
[55] Leslie Roberts,et al. A Proof of Principle , 2007, Science.
[56] J. Engelman,et al. Breast cancer-associated PIK3CA mutations are oncogenic in mammary epithelial cells. , 2005, Cancer research.
[57] S Matsuno,et al. Functional evaluation of PTEN missense mutations using in vitro phosphoinositide phosphatase assay. , 2000, Cancer research.
[58] C Eng,et al. Mutation spectrum and genotype-phenotype analyses in Cowden disease and Bannayan-Zonana syndrome, two hamartoma syndromes with germline PTEN mutation. , 1998, Human molecular genetics.
[59] A. Jemal,et al. Cancer statistics, 2019 , 2019, CA: a cancer journal for clinicians.
[60] M. Scaltriti,et al. Mechanisms of Resistance to PI3K and AKT Inhibitors , 2018 .
[61] Y. Yarden,et al. Resistance to Anti-Cancer Therapeutics Targeting Receptor Tyrosine Kinases and Downstream Pathways , 2018, Resistance to Targeted Anti-Cancer Therapeutics.
[62] Steven J. M. Jones,et al. Comprehensive molecular portraits of human breast tumours , 2013 .
[63] Adrian V. Lee,et al. Proteomic and transcriptomic profiling reveals a link between the PI3K pathway and lower estrogen-receptor (ER) levels and activity in ER+ breast cancer , 2010, Breast Cancer Research.
[64] S. Goodman,et al. Circulating mutant DNA to assess tumor dynamics , 2008, Nature Medicine.
[65] S. Hilsenbeck,et al. Proteomic and transcriptomic profiling reveals a link between the PI3K pathway and lower estrogen-receptor (ER) levels and activity in ER+ breast cancer , 2010, Breast Cancer Research.
[66] N. Dubrawsky. Cancer statistics , 2022 .