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

Reviving oncogenic addiction to MET bypassed by BRAF (G469A) mutation

17 Sept 2018

Abstract excerpt

Cancer clonal evolution is based on accrual of driving genetic alterations that are expected to cooperate and progressively increase malignancy. Little is known on whether any genetic alteration can hinder the oncogenic function of a coexisting alteration, so that therapeutic targeting of the one can, paradoxically, revive the function of the other. We report the case of a driver oncogene (MET) that is not only...

Read the complete abstract on PubMed

Topics

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

Share to Cancer-related Molecular Pathways
Share to Melanoma and MAPK Pathways
Share to PI3K/AKT/mTOR signaling in cancer

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 30224486
DOI: 10.1073/pnas.1721147115

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Reviving oncogenic addiction to MET bypassed by BRAF (G469A) mutationPMID 30224486Read ↗

MET-Driven Resistance to Dual EGFR and BRAF Blockade May Be Overcome by Switching from EGFR to MET Inhibition in BRAF-Mutated Colorectal Cancer.Semantic proximity Read ↗

Targeting MET Dysregulation in CancerSemantic proximity Read ↗

The GIST paradigm: lessons for other kinase‐driven cancersSemantic proximity Read ↗

Untying the gordion knot of targeting MET in cancer.Semantic proximity Read ↗

The multiple paths towards MET receptor addiction in cancer.Semantic proximity Read ↗

Exploiting signaling rewiring in cancer cells with co-existing oncogenic drivers.Semantic proximity Read ↗

Targeting MET amplification in Gastro-oesophageal (GO) malignancies and overcoming MET inhibitor resistance: challenges and opportunities.Semantic proximity Read ↗

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

The TICking clock of EGFR therapy resistance in glioblastoma: Target Independence or target CompensationSemantic proximity Read ↗

MYC and MET cooperatively drive hepatocellular carcinoma with distinct molecular traits and vulnerabilitiesSemantic proximity Read ↗

MYC and MET cooperatively drive hepatocellular carcinoma with distinct molecular traits and vulnerabilitiesSemantic proximity Read ↗

Activity and Resistance of a Brain-Permeable Paradox Breaker BRAF Inhibitor in Melanoma Brain Metastasis.Semantic proximity Read ↗

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