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Crizotinib-Resistant MET Mutations in Gastric Cancer Patients are Sensitive to Type II Tyrosine Kinase Inhibitors

https://doi.org/10.2217/fon-2019-0140
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What this work says

Outgoing claims: the papers this work cites, builds on, or argues with.

inferredcites →https://doi.org/10.1002/cncr.28454openalex-snapshot
MET amplification is not rare and predicts unfavorable clinical outcomes in patients with recurrent/metastatic gastric cancer after chemotherapy
inferredcites →https://doi.org/10.1007/s10120-015-0545-5openalex-snapshot
MET overexpression and amplification define a distinct molecular subgroup for targeted therapies in gastric cancer
inferredcites →https://doi.org/10.1016/j.jtho.2016.09.119openalex-snapshot
Emergence of Preexisting MET Y1230C Mutation as a Resistance Mechanism to Crizotinib in NSCLC with MET Exon 14 Skipping
inferredcites →https://doi.org/10.1016/j.jtho.2017.10.028openalex-snapshot
Osimertinib and Cabozantinib Combinatorial Therapy in an EGFR -Mutant Lung Adenocarcinoma Patient with Multiple MET Secondary-Site Mutations after Resistance to Crizotinib
inferredcites →https://doi.org/10.1016/s1470-2045(11)70232-7openalex-snapshot
Effect of crizotinib on overall survival in patients with advanced non-small-cell lung cancer harbouring ALK gene rearrangement: a retrospective analysis
inferredcites →https://doi.org/10.1021/jm2007613openalex-snapshot
Structure Based Drug Design of Crizotinib (PF-02341066), a Potent and Selective Dual Inhibitor of Mesenchymal–Epithelial Transition Factor (c-MET) Kinase and Anaplastic Lymphoma Kinase (ALK)
inferredcites →https://doi.org/10.1021/jm401427copenalex-snapshot
Targeting Receptor Tyrosine Kinase MET in Cancer: Small Molecule Inhibitors and Clinical Progress
inferredcites →https://doi.org/10.1038/bjc.2012.237openalex-snapshot
MET in gastric carcinomas: comparison between protein expression and gene copy number and impact on clinical outcome
inferredcites →https://doi.org/10.1038/bjc.2014.61openalex-snapshot
HER2, MET and FGFR2 oncogenic driver alterations define distinct molecular segments for targeted therapies in gastric carcinoma
inferredcites →https://doi.org/10.1038/modpathol.2015.33openalex-snapshot
Semi-comprehensive analysis of gene amplification in gastric cancers using multiplex ligation-dependent probe amplification and fluorescence in situ hybridization
inferredcites →https://doi.org/10.1038/nrclinonc.2018.13openalex-snapshot
Erratum: Targeting c-MET in gastrointestinal tumours: rationale, opportunities and challenges
inferredcites →https://doi.org/10.1056/nejmoa1006448openalex-snapshot
Anaplastic Lymphoma Kinase Inhibition in Non–Small-Cell Lung Cancer
inferredcites →https://doi.org/10.1056/nejmoa1406766openalex-snapshot
Crizotinib in ROS1-Rearranged Non–Small-Cell Lung Cancer
inferredcites →https://doi.org/10.1073/pnas.84.18.6379openalex-snapshot
Sequence of MET protooncogene cDNA has features characteristic of the tyrosine kinase family of growth-factor receptors.
inferredcites →https://doi.org/10.1093/annonc/mdx324openalex-snapshot
Combination therapy of erlotinib/crizotinib in a lung adenocarcinoma patient with primaryEGFR mutation plus secondaryMET amplification and a novel acquired crizotinib-resistant mutationMET G1108C
inferredcites →https://doi.org/10.1097/jto.0b013e31821528d3openalex-snapshot
Activity of Crizotinib (PF02341066), a Dual Mesenchymal-Epithelial Transition (MET) and Anaplastic Lymphoma Kinase (ALK) Inhibitor, in a Non-small Cell Lung Cancer Patient with De Novo MET Amplification
inferredcites →https://doi.org/10.1128/mcb.7.2.921openalex-snapshot
Characterization of the Rearranged tpr-met Oncogene Breakpoint
inferredcites →https://doi.org/10.1158/0008-5472.can-11-3490openalex-snapshot
The MET Oncogene Is a Functional Marker of a Glioblastoma Stem Cell Subtype
inferredcites →https://doi.org/10.1158/1078-0432.ccr-14-0450openalex-snapshot
MET Amplification Status in Therapy-Naïve Adeno- and Squamous Cell Carcinomas of the Lung
inferredcites →https://doi.org/10.1158/1078-0432.ccr-14-1293openalex-snapshot
Analysis of 1,115 Patients Tested for MET Amplification and Therapy Response in the MD Anderson Phase I Clinic
inferredcites →https://doi.org/10.1158/1078-0432.ccr-16-1789openalex-snapshot
A Phase I/II Multicenter Study of Single-Agent Foretinib as First-Line Therapy in Patients with Advanced Hepatocellular Carcinoma
inferredcites →https://doi.org/10.1158/1078-0432.ccr-16-3273openalex-snapshot
Acquired MET Y1248H and D1246N Mutations Mediate Resistance to MET Inhibitors in Non–Small Cell Lung Cancer
inferredcites →https://doi.org/10.1158/1538-7445.am2018-5807openalex-snapshot
Abstract 5807: The dual c-Met/VEGFR2 inhibitor foretinib augments chemotherapy response in preclinical models of gastric cancer
inferredcites →https://doi.org/10.1158/2159-8290.cd-16-0686openalex-snapshot
Acquired MET D1228V Mutation and Resistance to MET Inhibition in Lung Cancer
inferredcites →https://doi.org/10.1200/jco.2011.35.4928openalex-snapshot
MET Amplification Identifies a Small and Aggressive Subgroup of Esophagogastric Adenocarcinoma With Evidence of Responsiveness to Crizotinib
inferredcites →https://doi.org/10.1371/journal.pone.0054014openalex-snapshot
Phase II Study Evaluating 2 Dosing Schedules of Oral Foretinib (GSK1363089), cMET/VEGFR2 Inhibitor, in Patients with Metastatic Gastric Cancer
inferredcites →https://doi.org/10.18632/genesandcancer.96openalex-snapshot
Prognostic impact of KRAS mutant type and MET amplification in metastatic and recurrent gastric cancer patients treated with first-line S-1 plus cisplatin chemotherapy
inferredcites →https://doi.org/10.18632/oncotarget.10559openalex-snapshot
MET amplification in metastatic colorectal cancer: an acquired response to EGFR inhibition, not a de novo phenomenon
inferredcites →https://doi.org/10.18632/oncotarget.15457openalex-snapshot
Circulating tumor DNA profiling by next generation sequencing reveals heterogeneity of crizotinib resistance mechanisms in a gastric cancer patient with MET amplification
inferredcites →https://doi.org/10.18632/oncotarget.18753openalex-snapshot
A phase I study of foretinib plus erlotinib in patients with previously treated advanced non-small cell lung cancer: Canadian cancer trials group IND.196
inferredcites →https://doi.org/10.4251/wjgo.v7.i11.317openalex-snapshot
Clinical significance of MET in gastric cancer

What points at this work

Incoming claims: where this work appears in other papers’ reference lists and arguments.

inferred← citeshttps://doi.org/10.2139/ssrn.3501844openalex-extracted
inferred← citeshttps://doi.org/10.1007/s11684-022-0976-4openalex-snapshot
Treatment of advanced non-small cell lung cancer with driver mutations: current applications and future directions
inferred← citeshttps://doi.org/10.1038/s41392-022-01190-wopenalex-snapshot
Signaling pathways and therapeutic interventions in gastric cancer
inferred← citeshttps://doi.org/10.1080/17474124.2022.2093185openalex-snapshot
Targeting MET amplification in Gastro-oesophageal (GO) malignancies and overcoming MET inhibitor resistance: challenges and opportunities
inferred← citeshttps://doi.org/10.1101/2025.03.31.646490openalex-snapshot
Attention Guided Mechanism Interpretable Drug-Gene Interaction (MIDI) Modeling for Cancer Drug Response Prediction and Target Effect Explanation
inferred← citeshttps://doi.org/10.1158/2159-8290.cd-20-0571openalex-snapshot
TRK xDFG Mutations Trigger a Sensitivity Switch from Type I to II Kinase Inhibitors
inferred← citeshttps://doi.org/10.3389/fonc.2021.738832openalex-snapshot
Case Report: Sequential Combination Targeted Therapy With Type I and II MET Inhibitors in a Metastatic EGFR-Mutated, MET-Amplified NSCLC Patient With Acquired MET Y1230H Mutation
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