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Article

The PI3K/AKT pathway promotes gefitinib resistance in mutant KRAS lung adenocarcinoma by a deacetylase-dependent mechanism.

International journal of cancer - 1 Jun 2014

Jeannot Victor, Busser Benoît, Brambilla Elisabeth, Wislez Marie, Robin Blaise, Cadranel Jacques, Coll Jean-Luc, Hurbin Amandine

Abstract excerpt

To select the appropriate patients for treatment with epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), it is important to gain a better understanding of the intracellular pathways leading to EGFR-TKI resistance, which is a common problem in patients with lung cancer. We re...

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Share to Adenocarcinoma, Mucinous
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 24374738
DOI: 10.1002/ijc.28594

Genes

BAX
KRAS
EGFR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-24374738-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

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

Related research

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The PI3K/AKT pathway promotes gefitinib resistance in mutant KRAS lung adenocarcinoma by a deacetylase-dependent mechanism.PMID 24374738Read ↗

Gefitinib-sensitizing EGFR mutations in lung cancer activate anti-apoptotic pathways.Semantic proximity Read ↗

Convergent Akt activation drives acquired EGFR inhibitor resistance in lung cancer.Semantic proximity Read ↗

AKT inhibition synergistically enhances growth-inhibitory effects of gefitinib and increases apoptosis in non-small cell lung cancer cell lines.Semantic proximity Read ↗

PAK1 Is a Novel Therapeutic Target in Tyrosine Kinase Inhibitor-Resistant Lung Adenocarcinoma Activated by the PI3K/AKT Signaling Regardless of EGFR Mutation.Semantic proximity Read ↗

Interaction between p53 and Ras signaling controls cisplatin resistance via HDAC4- and HIF-1α-mediated regulation of apoptosis and autophagySemantic proximity Read ↗

Gefitinib (IRESSA) sensitive lung cancer cell lines show phosphorylation of Akt without ligand stimulationSemantic proximity Read ↗

Preclinical rationale for PI3K/Akt/mTOR pathway inhibitors as therapy for epidermal growth factor receptor inhibitor-resistant non-small-cell lung cancer.Semantic proximity Read ↗

Phosphorylation switches Bax from promoting to inhibiting apoptosis thereby increasing drug resistance.Semantic proximity Read ↗

The HSP90 inhibitor, NVP-AUY922, attenuates intrinsic PI3K inhibitor resistance in KRAS-mutant non-small cell lung cancer.Semantic proximity Read ↗

Mcl-1 Interacts with Akt to Promote Lung Cancer ProgressionSemantic proximity Read ↗

<i>AKT1</i> Amplification Regulates Cisplatin Resistance in Human Lung Cancer Cells through the Mammalian Target of Rapamycin/p70S6K1 PathwaySemantic proximity Read ↗

Enhanced cytotoxicity induced by gefitinib and specific inhibitors of the Ras or phosphatidyl inositol-3 kinase pathways in non-small cell lung cancer cells.Semantic proximity Read ↗

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