Epithelial-to-Mesenchymal Transition Antagonizes Response to Targeted Therapies in Lung Cancer by Suppressing BIM.

doi:10.1158/1078-0432.CCR-17-1577

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

Community

Back to search

Article

Epithelial-to-Mesenchymal Transition Antagonizes Response to Targeted Therapies in Lung Cancer by Suppressing BIM.

Clinical cancer research : an official journal of the American Association for Cancer Research - 1 Jan 2018

Song Kyung-A, Niederst Matthew J, Lochmann Timothy L, Hata Aaron N, Kitai Hidenori, Ham Jungoh, Floros Konstantinos V, Hicks Mark A, Hu Haichuan, Mulvey Hillary E, Drier Yotam, Heisey Daniel A R, Hughes Mark T, Patel Neha U, Lockerman Elizabeth L, Garcia Angel, Gillepsie Shawn, Archibald Hannah L, Gomez-Caraballo Maria, Nulton Tara J, Windle Brad E, Piotrowska Zofia, Sahingur Sinem E, Taylor Shirley M, Dozmorov Mikhail, Sequist Lecia V, Bernstein Bradley, Ebi Hiromichi, Engelman Jeffrey A, Faber Anthony C

Abstract excerpt

Purpose: Epithelial-to-mesenchymal transition (EMT) confers resistance to a number of targeted therapies and chemotherapies. However, it has been unclear why EMT promotes resistance, thereby impairing progress to overcome it.Experimental Design: We have developed several models of EMT-mediated resistance to EGFR inhibitors (EGFRi) in EGFR-mutant lung cancers to evaluate a novel mechanism of EMT-mediated...

Read the complete abstract on PubMed

Topics

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

Share to Aniline Compounds

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Bcl-2-Like Protein 11

Share to Cell Cycle

Share to Drug Resistance, Neoplasm

Share to Epithelial-Mesenchymal Transition

Share to Molecular Targeted Therapy

Share to RNA, Small Interfering

Share to Sulfonamides

Source

Open in PubMed Open full text

Identifiers

PMID: 29051323
DOI: 10.1158/1078-0432.CCR-17-1577
PMCID: PMC5959009

Genes

EGFR
ZEB1
KRAS

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

Epithelial-to-Mesenchymal Transition Antagonizes Response to Targeted Therapies in Lung Cancer by Suppressing BIM.PMID 29051323Read ↗

BIM mediates EGFR tyrosine kinase inhibitor-induced apoptosis in lung cancers with oncogenic EGFR mutations.Semantic proximity Read ↗

Epithelial-to-mesenchymal transition is a resistance mechanism to sequential MET-TKI treatment of MET-amplified EGFR-TKI resistant non-small cell lung cancer cellsSemantic proximity Read ↗

The role of epithelial to mesenchymal transition in resistance to epidermal growth factor receptor tyrosine kinase inhibitors in non-small cell lung cancerSemantic proximity Read ↗

Clinical significance of epidermal growth factor receptor tyrosine kinase inhibitors: sensitivity and resistance.Semantic proximity Read ↗

Induction of BIM is essential for apoptosis triggered by EGFR kinase inhibitors in mutant EGFR-dependent lung adenocarcinomas.Semantic proximity Read ↗

The Impact of Bevacizumab and miR200c on EMT and EGFR-TKI Resistance in EGFR-Mutant Lung Cancer Organoids.Semantic proximity Read ↗

The TGFβ-miR200-MIG6 pathway orchestrates the EMT-associated kinase switch that induces resistance to EGFR inhibitors.Semantic proximity Read ↗

Epithelial-to-Mesenchymal Transition Is a Mechanism of ALK Inhibitor Resistance in Lung Cancer Independent of ALK Mutation StatusSemantic proximity Read ↗

Prognostic Value of BIM Deletion in EGFR-Mutant NSCLC Patients Treated with EGFR-TKIs: A Meta-Analysis.Semantic proximity Read ↗

EGFR-TKI resistance due to BIM polymorphism can be circumvented in combination with HDAC inhibition.Semantic proximity Read ↗

ZEB1 Mediates Acquired Resistance to the Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitors in Non-Small Cell Lung Cancer.Semantic proximity Read ↗

Failure to EGFR-TKI-based therapy and tumoural progression are promoted by MEOX2/GLI1-mediated epigenetic regulation of EGFR in the human lung cancerSemantic proximity Read ↗

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