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

Drug tolerance and persistence to EGFR inhibitor treatment are mediated by an ILK-SFK-YAP signaling axis in lung adenocarcinoma

31 May 2025

Abstract excerpt

Combating resistance to targeted therapy remains a major challenge to improving lung cancer care. Epithelial-mesenchymal transition (EMT) in tumour cells is an established non-genetic resistance mechanism to EGFR tyrosine kinase inhibitors (TKI) that is also associated with worse outcome in patients. Here we demonstrate that integrin-linked kinase (ILK) is an important driver of EMT-mediated TKI resistance in...

Read the complete abstract on PubMed

Topics

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

Share to Cancer-related gene regulation
Share to Hippo pathway signaling and YAP/TAZ
Share to Lung Cancer Treatments and Mutations

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 40450112
DOI: 10.1038/s41388-025-03461-6

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Drug tolerance and persistence to EGFR inhibitor treatment are mediated by an ILK-SFK-YAP signaling axis in lung adenocarcinomaPMID 40450112Read ↗

ASCL1 Drives Tolerance to Osimertinib in EGFR Mutant Lung Cancer in Permissive Cellular Contexts.Semantic proximity Read ↗

Acquired resistance to KRAS G12C small-molecule inhibitors via genetic/nongenetic mechanisms in lung cancer.Semantic proximity Read ↗

The EGFR-STYK1-FGF1 axis sustains functional drug tolerance to EGFR inhibitors in EGFR-mutant non-small cell lung cancerSemantic proximity Read ↗

CRISPR screens reveal YAP/TEAD axis as a mediator of drug-tolerant cells in EGFR-mutant NSCLC.Semantic proximity Read ↗

The EGFR-STYK1-FGF1 axis sustains functional drug tolerance to EGFR inhibitors in EGFR-mutant non-small cell lung cancer.Semantic proximity Read ↗

Dissecting signaling regulators driving AXL-mediated bypass resistance and associated phenotypes by phosphosite perturbationsSemantic proximity Read ↗

Treatment-Induced Tumor Dormancy through YAP-Mediated Transcriptional Reprogramming of the Apoptotic Pathway.Semantic proximity Read ↗

Complementary modes of resistance to <i>EGFR</i> TKI in lung adenocarcinoma through MAPK activation and cellular plasticitySemantic proximity Read ↗

Activation of an AKT/FOXM1/STMN1 pathway drives resistance to tyrosine kinase inhibitors in lung cancer.Semantic proximity Read ↗

Tumor Cell Spatial Organization Directs EGFR/RAS/RAF Pathway Primary Therapy Resistance through YAP SignalingSemantic proximity Read ↗

GSTA1 Conferred Tolerance to Osimertinib and Provided Strategies to Overcome Drug-Tolerant Persister in EGFR-Mutant Lung Adenocarcinoma.Semantic proximity Read ↗

CRISPR Screens Reveal YAP/TEAD Axis as a Mediator of Drug-Tolerant Cells in EGFR- Mutant NSCLCSemantic proximity Read ↗

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