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Article

PIK3CA hotspot mutations differentially impact responses to MET targeting in MET-driven and non-driven preclinical cancer models.

Molecular cancer - 22 May 2017

Nisa Lluís, Häfliger Pascal, Poliaková Michaela, Giger Roland, Francica Paola, Aebersold Daniel Matthias, Charles Roch-Philippe, Zimmer Yitzhak, Medová Michaela

Abstract excerpt

BACKGROUND: The MET receptor tyrosine kinase represents a promising target in cancer. PIK3CA activating mutations are common in several tumor types and can potentially confer resistance to anti-receptor tyrosine kinase therapy. METHODS: MET and/or PI3K pathway inhibition was assessed in NIH3T3 cells harboring MET-activating point mutation with or without ectopic expression of PIK3CAE545K and PIK3CAH1047R, as well...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 28532501
DOI: 10.1186/s12943-017-0660-5
PMCID: PMC5441085

Genes

MET

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

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