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Article

Lack of AKT activation in lung cancer cells with EGFR mutation is a novel marker of cetuximab sensitivity.

Cancer biology & therapy - 1 Apr 2012

Takata Miyako, Chikumi Hiroki, Miyake Naomi, Adachi Kaori, Kanamori Yasunobu, Yamasaki Akira, Igishi Tadashi, Burioka Naoto, Nanba Eiji, Shimizu Eiji

Abstract excerpt

Epidermal growth factor receptor (EGFR) mutation is the best marker of sensitivity to the EGFR tyrosine kinase inhibitor gefitinib, but a marker for the anti-EGFR antibody cetuximab has not been identified in lung cancer. The present study investigated markers for sensitivity to cetuximab. Sensit...

Read the complete abstract on PubMed

Topics

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Share to Antibodies, Monoclonal, Humanized
Share to Cetuximab
Share to Gefitinib

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Dosage

Share to Genes, ras

Share to Proto-Oncogene Proteins c-akt

Share to Quinazolines

Share to STAT3 Transcription Factor

Source

Identifiers

PMID: 22313637
DOI: 10.4161/cbt.19238

Genes

EGFR
KRAS
STAT3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-22313637-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

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Lack of AKT activation in lung cancer cells with EGFR mutation is a novel marker of cetuximab sensitivity.PMID 22313637Read ↗

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