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

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

Cancer research - 15 Apr 2013

Nakagawa Takayuki, Takeuchi Shinji, Yamada Tadaaki, Ebi Hiromichi, Sano Takako, Nanjo Shigeki, Ishikawa Daisuke, Sato Mitsuo, Hasegawa Yoshinori, Sekido Yoshitaka, Yano Seiji

Abstract excerpt

BIM (BCL2L11) is a BH3-only proapoptotic member of the Bcl-2 protein family. BIM upregulation is required for apoptosis induction by EGF receptor (EGFR) tyrosine kinase inhibitors (EGFR-TKI) in EGFR-mutant forms of non-small cell lung cancer (NSCLC). Notably, a BIM deletion polymorphism occurs naturally in 12.9% of East Asian individuals, impairing the generation of the proapoptotic isoform required for the...

Read the complete abstract on PubMed

Topics

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

Share to Apoptosis Regulatory Proteins
Share to Bcl-2-Like Protein 11

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Gefitinib

Share to Histone Deacetylase Inhibitors

Share to Hydroxamic Acids

Share to Quinazolines

Share to Tumor Burden

Share to Vorinostat

Source

Identifiers

PMID: 23382048
DOI: 10.1158/0008-5472.CAN-12-3479

Genes

EGFR
EGF

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

EGFR-TKI resistance due to BIM polymorphism can be circumvented in combination with HDAC inhibition.PMID 23382048Read ↗

Phase I study of combined therapy with vorinostat and gefitinib to treat BIM deletion polymorphism-associated resistance in EGFR-mutant lung cancer (VICTROY-J): a study protocol.Semantic proximity Read ↗

A common BIM deletion polymorphism mediates intrinsic resistance and inferior responses to tyrosine kinase inhibitors in cancer.Semantic proximity Read ↗

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

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

BIM Gene Polymorphism Lowers the Efficacy of EGFR-TKIs in Advanced Nonsmall Cell Lung Cancer With Sensitive EGFR Mutations: A Systematic Review and Meta-Analysis.Semantic proximity Read ↗

The BIM deletion polymorphism is a prognostic biomarker of EGFR-TKIs response in NSCLC: A systematic review and meta-analysis.Semantic proximity Read ↗

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

Role of BIM Deletion Polymorphism and BIM Expression as Predictive Biomarkers to Maximize the Benefit of EGFR-TKI Treatment in EGFR-Positive NSCLC.Semantic proximity Read ↗

The Bim deletion polymorphism clinical profile and its relation with tyrosine kinase inhibitor resistance in Chinese patients with non-small cell lung cancer.Semantic proximity Read ↗

EGFR Inhibitors Plus Bevacizumab are Superior Than EGFR Inhibitors Alone as First-Line Setting in Advanced NSCLC With EGFR Mutations and BIM Deletion Polymorphisms (BIM-CLICaP).Semantic proximity Read ↗

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

Bcl-2-like protein 11 deletion polymorphism predicts survival in advanced non-small-cell lung cancer.Semantic proximity Read ↗

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