ArticleScientific reports2022
Co-occurrence CDK4/6 amplification serves as biomarkers of de novo EGFR TKI resistance in sensitizing EGFR mutation non-small cell lung cancer.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Systematic identification of genomic nonresponse biomarkers to cancer therapies.ESMO real world data and digital oncology · 2026Article
- Rewiring the Molecular Interplay of CDK4/6 Inhibitors in Lung Cancer: From Cell Cycle Control to Immune Microenvironment Remodeling.International journal of molecular sciences · 2026Review
- MET-amplified gastric cancers exhibit co-amplifications of BRAF, CDK6, and EGFR.The journal of pathology. Clinical research · 2026Article
- Patterns of central nervous system disease and molecular landscape in epidermal growth factor receptor exon 20 insertion mutated non-small cell carcinoma.Translational lung cancer research · 2026Article
- Epidermal growth factor receptor tyrosine kinase inhibitor for the treatment of non-small cell lung cancer in the past 30 years (1997-2026).Chinese medical journal · 2026Review
- Short-term response to alectinib and rapid progression in a lung squamous cell carcinoma patient harboring anTranslational cancer research · 2026Article
- The components and regulation of the Hippo pathway and its relationships with the progression and treatment of Non-small cell lung cancer (NSCLC).Cancer cell international · 2025Review
- Comparison of actionable alterations in cancers with kinase fusion, mutation, and copy number alteration.PloS one · 2025Article
- Genetic Alterations in HER2-Positive and Equivocal Breast Cancer by Immunohistochemistry.Breast cancer (Dove Medical Press) · 2025Article
- Osimertinib treatment response in a patient with lung adenocarcinoma harboring two rare EGFR mutations: A case report.Oncology letters · 2024Article
- Article
- Osimertinib and palbociclib in an EGFR-mutated NSCLC with primary CDK4 amplification after progression under osimertinib.NPJ precision oncology · 2024Article
- Next-generation sequencing reveals genetic heterogeneity and resistance mechanisms in patients withERJ open research · 2024Article
- NOTCH1 and CREBBP co-mutations negatively affect the benefit of adjuvant therapy in completely resected EGFR-mutated NSCLC: translational research of phase III IMPACT study.Molecular oncology · 2024Article
- CDK4/6 signaling attenuates the effect of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors inTranslational lung cancer research · 2023Article
- Exosome-derived circKIF20B suppresses gefitinib resistance and cell proliferation in non-small cell lung cancer.Cancer cell international · 2023Article
- Optimal therapy for concomitant EGFR and TP53 mutated non-small cell lung cancer: a real-world study.BMC cancer · 2023Article
- Genome-wide epigenetic and mRNA-expression profiling followed by CRISPR/Cas9-mediated gene-disruptions corroborate theTranslational lung cancer research · 2023Article
- Identification of afatinib-associated ADH1B and potential small-molecule drugs targeting ADH1B for hepatocellular carcinoma.Frontiers in pharmacology · 2023Article
- Discovery of new symmetrical and asymmetrical nitrile-containing 1,4-dihydropyridine derivatives as dual kinases and P-glycoprotein inhibitors: synthesis,Journal of enzyme inhibition and medicinal chemistry · 2022Article
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12 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Despite the development of predictive biomarkers to shape treatment paradigms and outcomes, de novo EGFR TKI resistance advanced non-small cell lung cancer (NSCLC) remains an issue of concern. We explored clinical factors in 332 advanced NSCLC who received EGFR TKI and molecular characteristics through 65 whole exome sequencing of various EGFR TKI responses including; de novo (progression within 3 months), intermediate response (IRs) and long-term response (LTRs) (durability > 2 years). Uncommon EGFR mutation subtypes were significantly variable enriched in de novo resistance. The remaining sensitizing EGFR mutation subtypes (exon 19 del and L858R) accounted for 75% of de novo resistance. Genomic landscape analysis was conducted, focusing in 10 frequent oncogenic signaling pathways with functional contributions; cell cycle, Hippo, Myc, Notch, Nrf2, PI-3-Kinase/Akt, RTK-RAS, TGF-β, p53 and β-catenin/Wnt signaling. Cell cycle pathway was the only significant alteration pathway among groups with the FDR p-value of 6 × 10
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