Ability of the Met kinase inhibitor crizotinib and new generation EGFR inhibitors to overcome resistance to EGFR inhibitors.
about
Tumor heterogeneity and resistance to EGFR-targeted therapy in advanced nonsmall cell lung cancer: challenges and perspectivesRoles of c-Met and RON kinases in tumor progression and their potential as therapeutic targetsALK inhibitors in non-small cell lung cancer: crizotinib and beyond.YangZheng XiaoJi exerts anti-tumour growth effects by antagonising the effects of HGF and its receptor, cMET, in human lung cancer cells.Effects of AKT inhibition on HGF-mediated erlotinib resistance in non-small cell lung cancer cell linesResistance to targeted cancer drugs through hepatocyte growth factor signalingMechanisms of resistance to EGFR tyrosine kinase inhibitors.Integrin α6β4 Promotes Autocrine Epidermal Growth Factor Receptor (EGFR) Signaling to Stimulate Migration and Invasion toward Hepatocyte Growth Factor (HGF).TC-N19, a novel dual inhibitor of EGFR and cMET, efficiently overcomes EGFR-TKI resistance in non-small-cell lung cancer cells.The coexistence of MET over-expression and an EGFR T790M mutation is related to acquired resistance to EGFR tyrosine kinase inhibitors in advanced non-small cell lung cancer.Clinical and comparative utility of afatinib in non-small cell lung cancer.Therapeutic strategies utilized in the setting of acquired resistance to EGFR tyrosine kinase inhibitors.The selective c-Met inhibitor tepotinib can overcome epidermal growth factor receptor inhibitor resistance mediated by aberrant c-Met activation in NSCLC models.Preclinical Evaluation of MET Inhibitor INC-280 With or Without the Epidermal Growth Factor Receptor Inhibitor Erlotinib in Non-Small-Cell Lung Cancer.Strategies for monitoring and combating resistance to combination kinase inhibitors for cancer therapy.Lung cancer as a paradigm for precision oncology in solid tumours.Valproic acid, an inhibitor of class I histone deacetylases, reverses acquired Erlotinib-resistance of lung adenocarcinoma cells: a Connectivity Mapping analysis and an experimental study.Data driven polypharmacological drug design for lung cancer: analyses for targeting ALK, MET, and EGFR.Mechanisms of resistance to irreversible epidermal growth factor receptor tyrosine kinase inhibitors and therapeutic strategies in non-small cell lung cancer.MET or NRAS amplification is an acquired resistance mechanism to the third-generation EGFR inhibitor naquotinib.Novel approaches against epidermal growth factor receptor tyrosine kinase inhibitor resistance.A phase I study of LY3164530, a bispecific antibody targeting MET and EGFR, in patients with advanced or metastatic cancer
P2860
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P2860
Ability of the Met kinase inhibitor crizotinib and new generation EGFR inhibitors to overcome resistance to EGFR inhibitors.
description
2013 nî lūn-bûn
@nan
2013 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2013 թվականի դեկտեմբերին հրատարակված գիտական հոդված
@hy
2013年の論文
@ja
2013年論文
@yue
2013年論文
@zh-hant
2013年論文
@zh-hk
2013年論文
@zh-mo
2013年論文
@zh-tw
2013年论文
@wuu
name
Ability of the Met kinase inhi ...... resistance to EGFR inhibitors.
@ast
Ability of the Met kinase inhi ...... resistance to EGFR inhibitors.
@en
type
label
Ability of the Met kinase inhi ...... resistance to EGFR inhibitors.
@ast
Ability of the Met kinase inhi ...... resistance to EGFR inhibitors.
@en
prefLabel
Ability of the Met kinase inhi ...... resistance to EGFR inhibitors.
@ast
Ability of the Met kinase inhi ...... resistance to EGFR inhibitors.
@en
P2093
P2860
P50
P1433
P1476
Ability of the Met kinase inhi ...... resistance to EGFR inhibitors
@en
P2093
Daisuke Ishikawa
Hiroshi Nishihara
Kazuo Yasumoto
Seiji Yano
Shigeki Nanjo
Shinji Takeuchi
Takako Sano
Takayuki Nakagawa
P2860
P304
P356
10.1371/JOURNAL.PONE.0084700
P407
P577
2013-12-26T00:00:00Z