Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

MET-EGFR dimerization in lung adenocarcinoma is dependent on EGFR mtations and altered by MET kinase inhibition.

PloS one - 1 Jan 2017

Ortiz-Zapater Elena, Lee Richard W, Owen William, Weitsman Gregory, Fruhwirth Gilbert, Dunn Robert G, Neat Michael J, McCaughan Frank, Parker Peter, Ng Tony, Santis George

Abstract excerpt

Advanced lung cancer has poor survival with few therapies. EGFR tyrosine kinase inhibitors (TKIs) have high response rates in patients with activating EGFR mutations, but acquired resistance is inevitable. Acquisition of the EGFR T790M mutation causes over 50% of resistance; MET amplification is also common. Preclinical data suggest synergy between MET and EGFR inhibitors. We hypothesized that EGFR-MET...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Adenocarcinoma of Lung
Share to Extracellular Signal-Regulated MAP Kinases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Focal Adhesion Protein-Tyrosine Kinases

Share to Mice, Inbred BALB C

Share to Mice, Nude

Share to Protein Multimerization

Share to Proto-Oncogene Proteins c-akt

Share to Proto-Oncogene Proteins c-met

Source

Open in PubMed Open full text

Identifiers

PMID: 28141869
DOI: 10.1371/journal.pone.0170798
PMCID: PMC5283661

Genes

EGFR
MET

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

MET-EGFR dimerization in lung adenocarcinoma is dependent on EGFR mtations and altered by MET kinase inhibition.PMID 28141869Read ↗

MET Dependence Oversteps EGFR Dependence via Balancing Dimerization of the Receptor Tyrosine Kinases in Osimertinib-Resistant MET-Amplified, EGFR-Mutated Non-Small Cell Lung Cancer.Semantic proximity Read ↗

Mechanistic insights into differential requirement of receptor dimerization for oncogenic activation of mutant EGFR and its clinical perspectiveSemantic proximity Read ↗

Mechanistic insights into the activation of oncogenic forms of EGF receptor.Semantic proximity Read ↗

Glioblastoma mutations impair ligand discrimination by EGFRSemantic proximity Read ↗

Drug-resistant EGFR mutations promote lung cancer by stabilizing interfaces in ligand-free kinase-active EGFR oligomers.Semantic proximity Read ↗

A Constitutive EGFR Kinase Dimer to Study Inhibitor Pharmacology.Semantic proximity Read ↗

Structural Differences between Wild-Type and Double Mutant EGFR Modulated by Third-Generation Kinase Inhibitors.Semantic proximity Read ↗

Glioblastoma mutations alter EGFR dimer structure to prevent ligand bias.Semantic proximity Read ↗

Complex relationship between ligand binding and dimerization in the epidermal growth factor receptor.Semantic proximity Read ↗

MET-GRB2 Signaling-Associated Complexes Correlate with Oncogenic MET Signaling and Sensitivity to MET Kinase Inhibitors.Semantic proximity Read ↗

EGFR Mutations in GBM Alter Ligand Binding and Subsequent Dimerization.Semantic proximity Read ↗

Enhanced dimerization drives ligand-independent activity of mutant epidermal growth factor receptor in lung cancer.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.