Multiple mutations and bypass mechanisms can contribute to development of acquired resistance to MET inhibitors. - Wikidata - wikimedia - TriplyDB

Multiple mutations and bypass mechanisms can contribute to development of acquired resistance to MET inhibitors.

Multiple mutations and bypass mechanisms can contribute to development of acquired resistance to MET inhibitors.

http://www.wikidata.org/entity/Q35525305

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Targeting the hepatocyte growth factor-cMET axis in cancer therapy c-Met as a Target for Personalized Therapy Clinical significance of MET in gastric cancer MET inhibitors in combination with other therapies in non-small cell lung cancer Structure-based methods for predicting target mutation-induced drug resistance and rational drug design to overcome the problem MET: a critical player in tumorigenesis and therapeutic target Molecular pathology of lung cancer: key to personalized medicine.Receptor tyrosine kinases fall into distinct classes based on their inferred signaling networks Parallel evolution under chemotherapy pressure in 29 breast cancer cell lines results in dissimilar mechanisms of resistance Hepatocyte growth factor sensitizes brain tumors to c-MET kinase inhibition.ERBB receptors: from oncogene discovery to basic science to mechanism-based cancer therapeutics.Circulating Tumor DNA Mutation Profiling by Targeted Next Generation Sequencing Provides Guidance for Personalized Treatments in Multiple Cancer Types Development of an in vitro model of acquired resistance to toceranib phosphate (Palladia®) in canine mast cell tumor.The potential roles of hepatocyte growth factor (HGF)-MET pathway inhibitors in cancer treatment.Emerging molecular targets in oncology: clinical potential of MET/hepatocyte growth-factor inhibitors.Effect of AXL on the epithelial-to-mesenchymal transition in non-small cell lung cancer.HGF/MET-directed therapeutics in gastroesophageal cancer: a review of clinical and biomarker development.Mechanisms of HGF/Met signaling to Brk and Sam68 in breast cancer progression.Targeting MET Amplification as a New Oncogenic Driver.Patient-derived models of acquired resistance can identify effective drug combinations for cancer.Fragment-based strategy for structural optimization in combination with 3D-QSAR.MiR-223 promotes the cisplatin resistance of human gastric cancer cells via regulating cell cycle by targeting FBXW7.Annotation of human cancers with EGFR signaling-associated protein complexes using proximity ligation assays MET amplification identifies a small and aggressive subgroup of esophagogastric adenocarcinoma with evidence of responsiveness to crizotinib.Complexity in the signaling network: insights from the use of targeted inhibitors in cancer therapy.Resistance to the c-Met inhibitor KRC-108 induces the epithelial transition of gastric cancer cells Suppression of tumor invasion and metastasis by concurrent inhibition of c-Met and VEGF signaling in pancreatic neuroendocrine tumors Genomic profiling of a Hepatocyte growth factor-dependent signature for MET-targeted therapy in glioblastoma.Piperlongumine and its analogs down-regulate expression of c-Met in renal cell carcinoma.PI3K-independent mTOR activation promotes lapatinib resistance and IAP expression that can be effectively reversed by mTOR and Hsp90 inhibition Activation of Pim Kinases Is Sufficient to Promote Resistance to MET Small-Molecule Inhibitors.Clinical Challenges to Current Molecularly Targeted Therapies in Lung Cancer Cytotoxic activity of tivantinib (ARQ 197) is not due solely to c-MET inhibition.HGF/Met and FOXM1 form a positive feedback loop and render pancreatic cancer cells resistance to Met inhibition and aggressive phenotypes.MET/HGF pathway activation as a paradigm of resistance to targeted therapies.Acquired resistance to dasatinib in lung cancer cell lines conferred by DDR2 gatekeeper mutation and NF1 loss.Acquired savolitinib resistance in non-small cell lung cancer arises via multiple mechanisms that converge on MET-independent mTOR and MYC activation.Potential therapeutic strategies to overcome acquired resistance to BRAF or MEK inhibitors in BRAF mutant cancers c-MET as a potential therapeutic target and biomarker in cancer.Targeting the Met pathway in lung cancer.

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P2860

Multiple mutations and bypass mechanisms can contribute to development of acquired resistance to MET inhibitors.

http://www.wikidata.org/entity/Q35525305

description

2011 nî lūn-bûn

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2011 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2011 թվականի հունվարին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

Multiple mutations and bypass ...... resistance to MET inhibitors.

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Multiple mutations and bypass ...... resistance to MET inhibitors.

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type

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Multiple mutations and bypass ...... resistance to MET inhibitors.

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Multiple mutations and bypass ...... resistance to MET inhibitors.

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Multiple mutations and bypass ...... resistance to MET inhibitors.

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Multiple mutations and bypass ...... resistance to MET inhibitors.

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0008-5472.CAN-10-1623

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Cancer Research

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Multiple mutations and bypass ...... resistance to MET inhibitors.

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P2093

Andrew Rogers

http://www.w3.org/2001/XMLSchema#string

Eugene Lifshits

http://www.w3.org/2001/XMLSchema#string

James G Christensen

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Jeffrey A Engelman

http://www.w3.org/2001/XMLSchema#string

Jie Qi

http://www.w3.org/2001/XMLSchema#string

Michele A McTigue

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P2860

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

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

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

c-Met inhibitors with novel binding mode show activity against several hereditary papillary renal cell carcinoma-related mutations

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

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

Met, metastasis, motility and more

Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias

The Met kinase inhibitor SU11274 exhibits a selective inhibition pattern toward different receptor mutated variants

The Met tyrosine kinase receptor in development and cancer

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1081-1091

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10.1158/0008-5472.CAN-10-1623

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21266357

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3208270

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