ArticlePloS one2017
Overall survival in EGFR mutated non-small-cell lung cancer patients treated with afatinib after EGFR TKI and resistant mechanisms upon disease progression.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- The role of miR-335-5p in the redifferentiation of BRAF p.V600E thyroid cancers.Molecular oncology · 2026Article
- Identification of potential inhibitors for drug-resistant EGFR mutations in non-small cell lung cancer using whole exome sequencing data.Frontiers in pharmacology · 2024Article
- Non-canonical integrin signaling activates EGFR and RAS-MAPK-ERK signaling in small cell lung cancer.Theranostics · 2023Article
- Identification of Ultrasound-Sensitive Prognostic Markers of LAML and Construction of Prognostic Risk Model Based on WGCNA.Journal of oncology · 2023Article
- Regulation of secretory pathway kinase or kinase-like proteins in human cancers.Frontiers in immunology · 2023Review
- Identifying General Tumor and Specific Lung Cancer Biomarkers by Transcriptomic Analysis.Biology · 2022Article
- Role of ErbB1 in the Underlying Mechanism of Lapatinib-Induced Diarrhoea: A Review.BioMed research international · 2022Review
- Pan-cancer analysis of advanced patient tumors reveals interactions between therapy and genomic landscapes.Nature cancer · 2020Article
- Article
- CircSEC31A Promotes the Malignant Progression of Non-Small Cell Lung Cancer Through Regulating SEC31A Expression via Sponging miR-376a.Cancer management and research · 2020Article
- Secretory Pathway KinaseOncoTargets and therapy · 2020Article
- Clinical and Prognostic Significance of Cell Sensitivity to Chemotherapy Detected in vitro on Treatment Response and Survival of Leukemia Patients.Journal of personalized medicine · 2019Article
- Article
- Notch3-dependent β-catenin signaling mediates EGFR TKI drug persistence in EGFR mutant NSCLC.Nature communications · 2018Article
- Crosstalk between VEGFR and other receptor tyrosine kinases for TKI therapy of metastatic renal cell carcinoma.Cancer cell international · 2018Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo determine survival in afatinib-treated patients after treatment with first-generation EGFR tyrosine kinase inhibitors (TKIs) and to study resistance mechanisms in afatinib-resistant tumors.
methodsCharacteristics and survival of patients treated with afatinib after resistance to erlotinib or gefitinib in two large Dutch centers were collected. Whole exome sequencing (WES) and pathway analysis was performed on available pre- and post-afatinib tumor biopsies and normal tissue.
resultsA total of 38 patients were treated with afatinib. T790M mutations were identified in 22/29 (76%) pre-afatinib treatment tumor samples. No difference in median progression-free-survival (2.8 months (95% CI 2.3-3.3) and 2.7 months (95% CI 0.9-4.6), p = 0.55) and median overall-survival (8.8 months (95% CI 4.2-13.4) and 3.6 months (95% CI 2.3-5.0), p = 0.14) were observed in T790M+ patients compared to T790M- mutations. Somatic mutations in TP53, ADAMTS2, CNN2 and multiple genes in the Wnt and PI3K-AKT pathway were observed in post-afatinib tumors of six afatinib-responding and in one non-responding patient. No new EGFR mutations were found in the post-afatinib samples of the six responding patients. Further analyses of post-afatinib progressive tumors revealed 28 resistant specific mutations in six genes (HLA-DRB1, AQP7, FAM198A, SEC31A, CNTLN, and ESX1) in three afatinib responding patients. No known EGFR-TKI resistant-associated copy number gains were acquired in the post-afatinib samples.
conclusionNo differences in survival were observed in patients with EGFR-T790M treated with afatinib compared to those without T790M. Tumors from patients who had progressive disease during afatinib treatment were enriched for mutations in genes involved in Wnt and PI3K-AKT pathways.
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