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

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

The American journal of pathology - 1 Sept 2012

Takeuchi Shinji, Wang Wei, Li Qi, Yamada Tadaaki, Kita Kenji, Donev Ivan S, Nakamura Takahiro, Matsumoto Kunio, Shimizu Eiji, Nishioka Yasuhiko, Sone Saburo, Nakagawa Takayuki, Uenaka Toshimitsu, Yano Seiji

Abstract excerpt

Acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) is a serious problem in the management of EGFR mutant lung cancer. We recently reported that hepatocyte growth factor (HGF) induces resistance to EGFR-TKIs by activating the Met/PI3K pathway. HGF is also known to induce angiogenesis in cooperation with vascular endothelial growth factor (VEGF), which is an important...

Read the complete abstract on PubMed

Topics

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

Share to Aminopyridines
Share to Antibody Specificity

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gefitinib

Share to Hepatocyte Growth Factor

Share to Neovascularization, Pathologic

Share to Proto-Oncogene Proteins c-met

Share to Quinazolines

Share to Vascular Endothelial Growth Factor Receptor-2

Source

Identifiers

PMID: 22789825
DOI: 10.1016/j.ajpath.2012.05.023

Genes

HGF
EGFR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Dual inhibition of Met kinase and angiogenesis to overcome HGF-induced EGFR-TKI resistance in EGFR mutant lung cancer.PMID 22789825Read ↗

TAK-701, a humanized monoclonal antibody to hepatocyte growth factor, reverses gefitinib resistance induced by tumor-derived HGF in non-small cell lung cancer with an EGFR mutation.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 ↗

Hepatocyte growth factor induces gefitinib resistance of lung adenocarcinoma with epidermal growth factor receptor-activating mutations.Semantic proximity Read ↗

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

Crizotinib overcomes hepatocyte growth factor-mediated resistance to gefitinib in EGFR-mutant non-small-cell lung cancer cells.Semantic proximity Read ↗

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 ↗

The hepatocyte growth factor/c-Met signaling pathway as a therapeutic target to inhibit angiogenesisSemantic proximity Read ↗

Targeting the c-Met Signaling Pathway in CancerSemantic proximity Read ↗

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

Single-Agent and Combination Therapeutic Strategies to Inhibit Hepatocyte Growth Factor/MET Signaling in CancerSemantic proximity Read ↗

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

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

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