Responsiveness of different MET tumour alterations to type I and type II MET inhibitors.

doi:10.1002/ctm2.70338

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

Community

Back to search

Article

Responsiveness of different MET tumour alterations to type I and type II MET inhibitors.

Clinical and translational medicine - 1 May 2025

Murciano-Goroff Yonina R, Foglizzo Valentina, Chang Jason, Rekhtman Natasha, Sisk Ann Elizabeth, Gibson Jamie, Judka Lia, Clemens Kristen, Roa Paola, Ahmed Shaza Sayed, Bremer Nicole V, Binaco Courtney Lynn, Muzungu Sherifah Kemigisha, Rodriguez Estelamari, Merrill Madeline, Sgroe Erica, Repetto Matteo, Stadler Zsofia K, Berger Michael F, Yu Helena A, Toska Eneda, Kannan Srinivasaraghavan, Verma Chandra S, Drilon Alexander, Cocco Emiliano

Abstract excerpt

BACKGROUND: Mutations in c-MET receptor tyrosine kinase (MET) can be primary oncogenic drivers of multiple tumour types or can be acquired as mechanisms of resistance to therapy. MET tyrosine kinase inhibitors (TKIs) are classified as type I or type II inhibitors, with the former binding to the DFG-in, active conformation of MET, and the latter to the DFG-out, inactive conformation of MET. Understanding how the...

Read the complete abstract on PubMed

Topics

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

Share to Anilides

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Drug Resistance, Neoplasm

Share to MET gene

Share to Mutation

Share to Neoplasms

Share to Protein Kinase Inhibitors

Share to Proto-Oncogene Proteins c-met

Share to Pyridines

Source

Open in PubMed Open full text

Identifiers

PMID: 40437874
DOI: 10.1002/ctm2.70338
PMCID: PMC12120261

Genes

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Responsiveness of different MET tumour alterations to type I and type II MET inhibitors.PMID 40437874Read ↗

Acquired METD1228V Mutation and Resistance to MET Inhibition in Lung Cancer.Semantic proximity Read ↗

NTRK kinase domain mutations in cancer variably impact sensitivity to type I and type II inhibitors.Semantic proximity Read ↗

Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET InhibitorsSemantic proximity Read ↗

Resistance to MET inhibition in MET-dependent NSCLC and therapeutic activity after switching from type I to type II MET inhibitors.Semantic proximity Read ↗

Targeting MET Dysregulation in CancerSemantic proximity Read ↗

Mutations in the MET tyrosine kinase domain and resistance to tyrosine kinase inhibitors in non-small-cell lung cancer.Semantic proximity Read ↗

Structural Alterations of MET Trigger Response to MET Kinase Inhibition in Lung Adenocarcinoma PatientsSemantic proximity Read ↗

MET-dependent solid tumours - molecular diagnosis and targeted therapy.Semantic proximity Read ↗

Glesatinib Exhibits Antitumor Activity in Lung Cancer Models and Patients Harboring MET Exon 14 Mutations and Overcomes Mutation-mediated Resistance to Type I MET Inhibitors in Nonclinical Models.Semantic proximity Read ↗

<i>MET</i> and <i>KRAS</i> Gene Amplification Mediates Acquired Resistance to MET Tyrosine Kinase InhibitorsSemantic proximity Read ↗

c-Met inhibitors with different binding modes: two is better than one.Semantic proximity Read ↗

Targeting MET: Discovery of Small Molecule Inhibitors as Non-Small Cell Lung Cancer Therapy.Semantic proximity Read ↗

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