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

Host-Dependent Phenotypic Resistance to EGFR Tyrosine Kinase Inhibitors.

Cancer research - 15 Jul 2021

Haga Yuya, Marrocco Ilaria, Noronha Ashish, Uribe Mary Luz, Nataraj Nishanth Belugali, Sekar Arunachalam, Drago-Garcia Diana, Borgoni Simone, Lindzen Moshit, Giri Suvendu, Wiemann Stefan, Tsutsumi Yasuo, Yarden Yosef

Abstract excerpt

Lung cancers driven by mutant forms of EGFR invariably develop resistance to kinase inhibitors, often due to secondary mutations. Here we describe an unconventional mechanism of resistance to dacomitinib, a newly approved covalent EGFR kinase inhibitor, and uncover a previously unknown step of resistance acquisition. Dacomitinib-resistant (DR) derivatives of lung cancer cells were established by means of...

Read the complete abstract on PubMed

Topics

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

Share to Mice
Share to Mice, Nude

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Phenotype

Share to Protein Kinase Inhibitors

Source

Open in PubMed Open full text

Identifiers

PMID: 33941614
DOI: 10.1158/0008-5472.CAN-20-3555
PMCID: PMC7611293

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

Host-Dependent Phenotypic Resistance to EGFR Tyrosine Kinase Inhibitors.PMID 33941614Read ↗

Acquired resistance mechanisms to tyrosine kinase inhibitors in lung cancer with activating epidermal growth factor receptor mutation--diversity, ductility, and destiny.Semantic proximity Read ↗

Primary Double-Strike Therapy for Cancers to Overcome EGFR Kinase Inhibitor Resistance: Proposal from the Bench.Semantic proximity Read ↗

Early Steps of Resistance to Targeted Therapies in Non-Small-Cell Lung CancerSemantic proximity Read ↗

Resiliency of lung cancers to EGFR inhibitor treatment unveiled, offering opportunities to divide and conquer EGFR inhibitor resistance.Semantic proximity Read ↗

Drug Tolerance to EGFR Tyrosine Kinase Inhibitors in Lung Cancers with EGFR Mutations.Semantic proximity Read ↗

Tumor cells can follow distinct evolutionary paths to become resistant to epidermal growth factor receptor inhibition.Semantic proximity Read ↗

Resistance of Lung Cancer to EGFR-Specific Kinase Inhibitors: Activation of Bypass Pathways and Endogenous MutatorsSemantic proximity Read ↗

Acquired resistance to EGFR inhibitors is associated with a manifestation of stem cell-like properties in cancer cells.Semantic proximity Read ↗

Tumor cell-intrinsic phenotypic plasticity facilitates adaptive cellular reprogramming driving acquired drug resistanceSemantic proximity Read ↗

Lung cancers with acquired resistance to EGFR inhibitors occasionally harbor <i>BRAF</i> gene mutations but lack mutations in <i>KRAS, NRAS,</i> or <i>MEK1</i>Semantic proximity Read ↗

Mechanisms of Acquired Resistance and Tolerance to EGFR Targeted Therapy in Non-Small Cell Lung CancerSemantic proximity Read ↗

Characterizing Evolutionary Dynamics Reveals Strategies to Exhaust the Spectrum of Subclonal Resistance in EGFR-Mutant Lung Cancer.Semantic proximity Read ↗

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