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

Effects of AKT inhibition on HGF-mediated erlotinib resistance in non-small cell lung cancer cell lines.

Journal of cancer research and clinical oncology - 1 Apr 2015

Holland William S, Chinn Danielle C, Lara Primo N, Gandara David R, Mack Philip C

Abstract excerpt

PURPOSE: Acquired resistance to erlotinib in patients with EGFR-mutant non-small cell lung cancer can result from aberrant activation of alternative receptor tyrosine kinases, such as the HGF-driven c-MET receptor. We sought to determine whether inhibition of AKT signaling could augment erlotinib activity and abrogate HGF-mediated resistance. METHODS: The effects of MK-2206, a selective AKT inhibitor, were...

Read the complete abstract on PubMed

Topics

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

Share to Hepatocyte Growth Factor
Share to Benzamides

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Cycle Checkpoints

Share to Drug Synergism

Share to Erlotinib Hydrochloride

Share to Heterocyclic Compounds, 3-Ring

Share to Mitogen-Activated Protein Kinase 1

Share to Mitogen-Activated Protein Kinase 3

Source

Open in PubMed Open full text

Identifiers

PMID: 25323938
DOI: 10.1007/s00432-014-1855-4
PMCID: PMC4562434

Genes

EGFR
HGF
KRAS
MET

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Effects of AKT inhibition on HGF-mediated erlotinib resistance in non-small cell lung cancer cell lines.PMID 25323938Read ↗

The novel phosphoinositide 3-kinase-mammalian target of rapamycin inhibitor, BEZ235, circumvents erlotinib resistance of epidermal growth factor receptor mutant lung cancer cells triggered by hepatocyte growth factor.Semantic proximity Read ↗

Met kinase inhibitor E7050 reverses three different mechanisms of hepatocyte growth factor-induced tyrosine kinase inhibitor resistance in EGFR mutant lung cancer.Semantic proximity Read ↗

mTOR inhibitors control the growth of EGFR mutant lung cancer even after acquiring resistance by HGF.Semantic proximity Read ↗

A combinatorial strategy for treating KRAS-mutant lung cancer.Semantic proximity Read ↗

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

Hepatocyte growth factor induces resistance to anti-epidermal growth factor receptor antibody in lung cancer.Semantic proximity Read ↗

Transient PI3K inhibition induces apoptosis and overcomes HGF-mediated resistance to EGFR-TKIs in EGFR mutant lung cancer.Semantic 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 ↗

Combined use of PI3K and MEK inhibitors synergistically inhibits lung cancer with EGFR and KRAS mutations.Semantic proximity Read ↗

Dual inhibition of MEK1/2 and EGFR synergistically induces caspase-3-dependent apoptosis in EGFR inhibitor-resistant lung cancer cells via BIM upregulation.Semantic proximity Read ↗

Norcantharidin combined with EGFR-TKIs overcomes HGF-induced resistance to EGFR-TKIs in EGFR mutant lung cancer cells via inhibition of Met/PI3k/Akt pathway.Semantic proximity Read ↗

Dual inhibition of Met kinase and angiogenesis to overcome HGF-induced EGFR-TKI resistance in EGFR mutant lung cancer.Semantic proximity Read ↗

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