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

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

Cancer research - 1 Feb 2011

Qi Jie, McTigue Michele A, Rogers Andrew, Lifshits Eugene, Christensen James G, Jänne Pasi A, Engelman Jeffrey A

Abstract excerpt

Therapies targeting receptor tyrosine kinases have shown efficacy in molecularly defined subsets of cancers. Unfortunately, cancers invariably develop resistance, and overcoming or preventing resistance will ultimately be key to unleashing their full therapeutic potential. In this study, we examined how cancers become resistant to MET inhibitors, a class of drugs currently under clinical development. We utilized...

Read the complete abstract on PubMed

Topics

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

Share to Crizotinib
Share to Extracellular Signal-Regulated MAP Kinases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to MAP Kinase Kinase Kinases

Share to Oncogene Protein v-akt

Share to Proto-Oncogene Proteins c-met

Share to Receptors, Growth Factor

Share to Sulfones

Share to Transforming Growth Factor alpha

Source

Open in PubMed Open full text

Identifiers

PMID: 21266357
DOI: 10.1158/0008-5472.CAN-10-1623
PMCID: PMC3208270

Genes

MET
EGFR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

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

Multiple mutations and bypass mechanisms can contribute to development of acquired resistance to MET inhibitors.PMID 21266357Read ↗

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

Acquired Resistance Mechanisms to Combination Met-TKI/EGFR-TKI Exposure in Met-Amplified EGFR-TKI-Resistant Lung Adenocarcinoma Harboring an Activating EGFR Mutation.Semantic proximity Read ↗

Anticancer drug resistance: An update and perspective.Semantic proximity Read ↗

Overcoming resistance to targeted therapy using MET inhibitors in solid cancers: evidence from preclinical and clinical studies.Semantic proximity Read ↗

Resistance to tyrosine kinase inhibitors: calling on extra forces.Semantic proximity Read ↗

Dual-Targeted Therapy Circumvents Non-Genetic Drug Resistance to Targeted TherapySemantic proximity Read ↗

[Mechanisms of resistance to target therapy].Semantic proximity Read ↗

Mechanisms of targeted therapy resistance take a de-TOR.Semantic proximity Read ↗

A Drug Resistance Screen Using a Selective MET Inhibitor Reveals a Spectrum of Mutations That Partially Overlap with Activating Mutations Found in Cancer PatientsSemantic proximity Read ↗

Dissecting mechanisms of resistance to targeted drug combination therapy in human colorectal cancerSemantic proximity Read ↗

The role of MET in chemotherapy resistanceSemantic proximity Read ↗

The clinical efficacy of combinatorial therapy of EGFR-TKI and crizotinib in overcoming MET amplification-mediated resistance from prior EGFR-TKI therapy.Semantic proximity Read ↗

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