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

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

Cancer letters - 10 Oct 2017

Park Kang-Seo, Yang Hannah, Choi Junyoung, Seo Seyoung, Kim Deokhoon, Lee Chang Hoon, Jeon Hanwool, Kim Sang-We, Lee Dae Ho

Abstract excerpt

More than 25% of non-small cell lung cancers (NSCLCs) carry mutations in KRAS, one of the most common oncogenic drivers in this disease. KRAS-mutant NSCLC responds poorly to currently available therapies; therefore, novel treatment strategies are needed. Here, we describe a particularly promising targeted therapeutic strategy against KRAS mutation-harboring NSCLC intrinsically resistant to treatment by PI3K...

Read the complete abstract on PubMed

Topics

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

Share to Antineoplastic Combined Chemotherapy Protocols
Share to Drug Resistance, Neoplasm

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to HSP90 Heat-Shock Proteins

Share to Isoxazoles

Share to Mice, Inbred BALB C

Share to Phosphoinositide-3 Kinase Inhibitors

Share to Protein Kinase Inhibitors

Share to Proto-Oncogene Proteins p21(ras)

Source

Identifiers

PMID: 28797845
DOI: 10.1016/j.canlet.2017.07.028

Genes

KRAS

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

The HSP90 inhibitor, NVP-AUY922, attenuates intrinsic PI3K inhibitor resistance in KRAS-mutant non-small cell lung cancer.PMID 28797845Read ↗

The HSP90 inhibitor, NVP-AUY922, sensitizes KRAS-mutant non-small cell lung cancer with intrinsic resistance to MEK inhibitor, trametinib.Semantic proximity Read ↗

Acquired Resistance to the Hsp90 Inhibitor, Ganetespib, in KRAS-Mutant NSCLC Is Mediated via Reactivation of the ERK-p90RSK-mTOR Signaling Network.Semantic proximity Read ↗

Targeting KRAS-mutant non-small cell lung cancer with the Hsp90 inhibitor ganetespib.Semantic proximity Read ↗

Dual Inhibitors of KRASG12D and HSP90 Are Effective against KRASG12D Inhibitor Resistance.Semantic proximity Read ↗

PIK3CA mutation as an acquired resistance driver to EGFR-TKIs in non-small cell lung cancer: Clinical challenges and opportunities.Semantic proximity Read ↗

WEE1 confers resistance to KRASG12C inhibitors in non-small cell lung cancer.Semantic proximity Read ↗

Epithelial-to-Mesenchymal Transition is a Cause of Both Intrinsic and Acquired Resistance to KRAS G12C Inhibitor in KRAS G12C-Mutant Non-Small Cell Lung Cancer.Semantic proximity Read ↗

The HSP90 inhibitor ganetespib potentiates the antitumor activity of EGFR tyrosine kinase inhibition in mutant and wild-type non-small cell lung cancer.Semantic proximity Read ↗

Molecular mechanisms of tumor resistance to PI3K-mTOR-targeted therapySemantic proximity Read ↗

Resistance to dual blockade of the kinases PI3K and mTOR in KRAS-mutant colorectal cancer models results in combined sensitivity to inhibition of the receptor tyrosine kinase EGFR.Semantic proximity Read ↗

Targeted Inhibition of the Molecular Chaperone Hsp90 Overcomes ALK Inhibitor Resistance in Non–Small Cell Lung CancerSemantic proximity Read ↗

Reactivation of the p90RSK-CDC25C Pathway Leads to Bypass of the Ganetespib-Induced G2-M Arrest and Mediates Acquired Resistance to Ganetespib in KRAS-Mutant NSCLC.Semantic proximity Read ↗

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