MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib - Wikidata - wikimedia - TriplyDB

MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib

MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib

http://www.wikidata.org/entity/Q24646295

about

EGFR/Met association regulates EGFR TKI resistance in breast cancer Perturbation of the mutated EGFR interactome identifies vulnerabilities and resistance mechanisms Trials to Overcome Drug Resistance to EGFR and ALK Targeted Therapies - Past, Present, and Future EGFR-mutant lung adenocarcinomas treated first-line with the novel EGFR inhibitor, XL647, can subsequently retain moderate sensitivity to erlotinib Molecular biology of lung cancer The MET axis as a therapeutic target.Molecular biology of lung cancer: clinical implications Impact of epidermal growth factor receptor and KRAS mutations on clinical outcomes in previously untreated non-small cell lung cancer patients: results of an online tumor registry of clinical trials An overview of the c-MET signaling pathway Targeting the PI3K signaling pathway in cancer Tyrosine Kinase Receptor Landscape in Lung Cancer: Therapeutical Implications Intrinsic resistance to EGFR tyrosine kinase inhibitors in advanced non-small-cell lung cancer with activating EGFR mutations Recent Advances in Targetable Therapeutics in Metastatic Non-Squamous NSCLC Understanding and Targeting MET Signaling in Solid Tumors - Are We There Yet?Biomarker development in MET-targeted therapy MicroRNA In Lung Cancer: Novel Biomarkers and Potential Tools for Treatment Molecular Pathology and Personalized Medicine: The Dawn of a New Era in Companion Diagnostics-Practical Considerations about Companion Diagnostics for Non-Small-Cell-Lung-Cancer Hepatocyte Growth Factor from a Clinical Perspective: A Pancreatic Cancer Challenge Targeted therapies for patients with advanced NSCLC harboring wild-type EGFR: what's new and what's enough Dysregulation of the Met pathway in non-small cell lung cancer: implications for drug targeting and resistance Tumor-Derived Cell Lines as Molecular Models of Cancer Pharmacogenomics MET inhibitors in combination with other therapies in non-small cell lung cancer The latest therapeutic strategies after resistance to first generation epidermal growth factor receptor tyrosine kinase inhibitors (EGFR TKIs) in patients with non-small cell lung cancer (NSCLC)The role of MET receptor tyrosine kinase in non-small cell lung cancer and clinical development of targeted anti-MET agents Predictive biomarkers in precision medicine and drug development against lung cancer Molecular testing in lung cancer in the era of precision medicine Molecular testing guideline for selection of lung cancer patients for EGFR and ALK tyrosine kinase inhibitors: guideline from the College of American Pathologists, International Association for the Study of Lung Cancer, and Association for Molecular EGFR mutations as a prognostic and predictive marker in non-small-cell lung cancer Management of acquired resistance to epidermal growth factor receptor kinase inhibitors in patients with advanced non-small cell lung cancer Irreversible EGFR-TKIs: dreaming perfection Resistance to receptor tyrosine kinase inhibition in cancer: molecular mechanisms and therapeutic strategies Review of the current targeted therapies for non-small-cell lung cancer Primary and acquired resistance to EGFR-targeted therapies in colorectal cancer: impact on future treatment strategies Signaling cross-talk in the resistance to HER family receptor targeted therapy Role of mesenchymal-epithelial transition amplification in resistance to anti-epidermal growth factor receptor agents Advances of molecular subtype and targeted therapy of lung cancer Abl Kinases Regulate HGF/Met Signaling Required for Epithelial Cell Scattering, Tubulogenesis and Motility Characterizing tyrosine phosphorylation signaling in lung cancer using SH2 profiling Phase II study evaluating 2 dosing schedules of oral foretinib (GSK1363089), cMET/VEGFR2 inhibitor, in patients with metastatic gastric cancer LY2801653 is an orally bioavailable multi-kinase inhibitor with potent activity against MET, MST1R, and other oncoproteins, and displays anti-tumor activities in mouse xenograft models

P2860

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P2860

MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib

http://www.wikidata.org/entity/Q24646295

description

2007 nî lūn-bûn

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2007 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2007 թվականի դեկտեմբերին հրատարակված գիտական հոդված

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2007年の論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年论文

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name

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MET amplification occurs with ...... ance to gefitinib or erlotinib

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PNAS.0710370104

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Proceedings of the National Academy of Sciences of the United States of America

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MET amplification occurs with ...... ance to gefitinib or erlotinib

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P2093

Adi Gazdar

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Agnes Viale

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Chih-Hsin Yang

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Dhananjay Chitale

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Gregory Riely

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James Bean

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Janos Szoke

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Jin-Yuan Shih

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Lu Wang

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Marissa Balak

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P2860

Sequence of MET protooncogene cDNA has features characteristic of the tyrosine kinase family of growth-factor receptors

High-resolution genomic profiles of human lung cancer

Amplification of MET may identify a subset of cancers with extreme sensitivity to the selective tyrosine kinase inhibitor PHA-665752

EGF receptor gene mutations are common in lung cancers from "never smokers" and are associated with sensitivity of tumors to gefitinib and erlotinib

Characterizing the cancer genome in lung adenocarcinoma.

Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain

EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy.

EGFR mutation and resistance of non-small-cell lung cancer to gefitinib.

Exon 19 deletion mutations of epidermal growth factor receptor are associated with prolonged survival in non-small cell lung cancer patients treated with gefitinib or erlotinib.

MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling.

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20932-7

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scholarly article

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578451

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10.1073/PNAS.0710370104

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52

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104

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Cameron Brennan

Valerie W Rusch

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2007-12-26T00:00:00Z

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5754996

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18093943

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2409244

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