ArticleNature communications2025
Basal-shift transformation leads to EGFR therapy-resistance in human lung adenocarcinoma.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Advantages and research progress of three-dimensional culture systems for lung cancer drug screening (Review).Oncology letters · 2026Review
- Metabolomics of Eryngium heterophyllum by UHPLC-QToF-MS and In Silico Insights Into Potential Metabolic Syndrome Targets.Chemistry & biodiversity · 2026Article
- Deconstructing cancer in 3D: models, mechanisms, and personalized solutions.Molecular cancer · 2026Review
- miR-542-3p targets TTF1 to regulate proliferation, invasion, and migration of lung adenocarcinoma via the MAPK signaling pathway.Scientific reports · 2026Article
- Artesunate Induces G0/G1 Phase Arrest in Tumor Cells and Associates With Cyclin-Dependent Kinase 4 (CDK4).Cancer medicine · 2026Article
- Bidirectional coupling among EMT, AXL-RB1 signaling and lineage switch drives resistance to osimertinib and worse clinical outcomes in NSCLC.bioRxiv : the preprint server for biology · 2026Article
- Tolerance and Resistance to Targeted Therapy in NSCLC: Emerging Concepts and Strategies.JTO clinical and research reports · 2026Review
- Lineage plasticity: a new dilemma in lung cancer treatment.Molecular biology reports · 2026Review
- A multi-algorithm machine learning framework identifies FGD5, LRRC36, C8B, and MYOC as novel diagnostic biomarkers in lung adenocarcinoma.Discover oncology · 2026Article
- Non-immobilized graphene oxide-based screening of aptamers for non-small cell lung cancer (NSCLC) drug resistance biomarkers and development of a nano-detection platform.Mikrochimica acta · 2026Article
- Squamous transformation of EGFR-mutant lung adenocarcinoma after EGFR-TKI therapy: clonal continuity, tissue-based diagnosis, and therapeutic evidence gaps.Frontiers in oncology · 2026Review
- Case Report: squamous transformation after long-term osimertinib in EGFR-mutant lung adenocarcinoma with retained EGFR/TP53 alterations.Frontiers in oncology · 2026Article
- Mitochondrial niches of residual disease in EGFR-mutant NSCLC: immune-constrained persistence and therapeutic interception.Frontiers in immunology · 2026Review
- Lung cancer organoids for functional precision oncology: from disease modeling to clinical decision support.Frontiers in oncology · 2026Review
- Article
- Osimertinib acquired resistance among patients with EGFR-mutated NSCLC: from molecular mechanisms to clinical therapeutic strategies.Cancer drug resistance (Alhambra, Calif.) · 2025Review
Corrections and comments
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Authors and funding
34 authors.
Funding
Abstract
Although EGFR tyrosine kinase inhibitors (EGFR-TKIs) are effective for EGFR-mutant lung adenocarcinoma (LUAD), resistance inevitably develops through diverse mechanisms, including secondary genetic mutations, amplifications and as-yet undefined processes. To comprehensively unravel the mechanisms of EGFR-TKI resistance, we establish a biobank of patient-derived EGFR-mutant lung cancer organoids, encompassing cases previously treated with EGFR-TKIs. Through comprehensive molecular profiling including single-cell analysis, here we identify a subgroup of EGFR-TKI-resistant LUAD organoids that lacks known resistance-related genetic lesions and instead exhibits a basal-shift phenotype characterized by the hybrid expression of LUAD- and squamous cell carcinoma-related genes. Prospective gene engineering demonstrates that NKX2-1 knockout induces the basal-shift transformation along with EGFR-target therapy resistance. Basal-shift LUADs frequently harbor CDKN2A/B loss and are sensitive to CDK4/6 inhibitors. Our EGFR-mutant lung cancer organoid library not only offers a valuable resource for lung cancer research but also provides insights into molecular underpinnings of EGFR-TKI resistance, facilitating the development of therapeutic strategies.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.