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

TP63 drives TKI resistance in EGFR-mutant lung cancer via ferroptosis inhibition.

Chinese clinical oncology - 1 Apr 2026

Li Kehan, Liu Jiane, Wang Wenjuan, Zhang Guangmin, Zhu Lina, Liu Linlin, Xu Xiaohui

Abstract excerpt

BACKGROUND: The emergence of acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) presents a significant obstacle in the therapeutic strategy for EGFR-mutant non-small cell lung cancer (NSCLC). While secondary mutations explain some cases, adaptive resistance mechanisms involving lineage plasticity and metabolic rewiring are increasingly recognized but poorly...

Topics

Join the communities discussing this publication.

Acrylamides
Drug Resistance, Neoplasm
ErbB Receptors
Ferroptosis
Indoles

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Protein Kinase Inhibitors

Tumor Suppressor Proteins

Source

Identifiers

PMID: 42145014
DOI: 10.21037/cco-2025-aw-151

Genes

TP63
EGFR
GPX4

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Community interpretation

Discuss the evidence

Ask a question, add context or challenge an interpretation. Community activity is separate from scientific evidence strength.

0

discussions

0

replies

Citations encouraged

Claims remain attributable.

No discussion yet

Be the first to add a careful, cited interpretation.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

TP63 drives TKI resistance in EGFR-mutant lung cancer via ferroptosis inhibition.PMID 42145014Read ↗

ΔNp63 Inhibits Oxidative Stress-Induced Cell Death, Including Ferroptosis, and Cooperates with the BCL-2 Family to Promote Clonogenic SurvivalSemantic proximity Read ↗

Identification of GPX4 as a therapeutic target for lung adenocarcinoma after EGFR-TKI resistanceSemantic proximity Read ↗

Ferroptosis response segregates small cell lung cancer (SCLC) neuroendocrine subtypesSemantic proximity Read ↗

Dysregulation of Labile Iron Predisposes Chemotherapy Resistant Cancer Cells to FerroptosisSemantic proximity Read ↗

Auranofin reveals therapeutic anticancer potential by triggering distinct molecular cell death mechanisms and innate immunity in mutant p53 non-small cell lung cancerSemantic proximity Read ↗

Osimertinib-tolerant lung cancer cells are susceptible to ferroptosis.Semantic proximity Read ↗

Mutant p53 protects triple-negative breast adenocarcinomas from ferroptosis in vivoSemantic proximity Read ↗

Inhibition of TPI1 Sensitizes Cisplatin-Resistant Oral Cancer to FerroptosisSemantic proximity Read ↗

Selenite as a dual apoptotic and ferroptotic agent synergizes with EGFR and KRAS inhibitors with epigenetic interference.Semantic proximity Read ↗

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

Identification of a set of genes potentially responsible for resistance to ferroptosis in lung adenocarcinoma cancer stem cellsSemantic proximity Read ↗

In vivo vulnerabilities to GPX4 and HDAC inhibitors in drug-persistent versus drug-resistant BRAFV600E lung adenocarcinoma.Semantic proximity Read ↗

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