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Article

KRAS mutant lung cancer cells are differentially responsive to MEK inhibitor due to AKT or STAT3 activation: implication for combinatorial approach.

Molecular carcinogenesis - 1 Apr 2010

Yoon Young-Kwang, Kim Hwang-Phill, Han Sae-Won, Oh Do Youn, Im Seock-Ah, Bang Yung-Jue, Kim Tae-You

Abstract excerpt

KRAS is frequently mutated in nonsmall cell lung cancer (NSCLC), resulting in the activation of the MAPK/ERK kinase (MEK)/ERK pathway. High-throughput mutation profile has shown that lung cancer frequently harbors comutation of cancer-related genes. Therefore, given that cancer cells have multiple genetic alterations, combinatorial therapeutic strategy is demanded for effective cancer therapy. To address this, we...

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Source

Identifiers

PMID: 20358631
DOI: 10.1002/mc.20607

Genes

KRAS
PTEN
STAT3
EGFR
JAK2

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.

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KRAS mutant lung cancer cells are differentially responsive to MEK inhibitor due to AKT or STAT3 activation: implication for combinatorial approach.PMID 20358631Read ↗

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