ArticleJournal of cancer research and clinical oncology2018
Whole-exome sequencing identifies key mutated genes in T790M wildtype/cMET-unamplified lung adenocarcinoma with acquired resistance to first-generation EGFR tyrosine kinase inhibitors.
Article in Journal of cancer research and clinical oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Early acquired resistance to EGFR-TKIs in lung adenocarcinomas before radiographic advanced identified by CT radiomic delta model based on two central studies.Scientific reports · 2023Article
- Cost-effectiveness analysis of dacomitinib versus gefitinib for the first-line therapy of patients with EGFR mutation-positive non-small-cell lung cancer in the United States and China.Annals of translational medicine · 2021Article
- Perspective: Cellular and Molecular Profiling Technologies in Personalized Oncology.Journal of personalized medicine · 2019Article
- The Role Of Circulating Tumor DNA In Therapeutic Resistance.OncoTargets and therapy · 2019Review
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Authors and funding
7 authors.
Funding
Abstract
purposeLung cancer is the leading cause of cancer-related death worldwide. Lung adenocarcinoma harboring EGFR-activating mutations will inevitably acquire resistance to first-generation EGFR tyrosine kinase inhibitors (TKIs). EGFR T790M mutation and cMET amplification are common mechanisms. Further study is needed to explore unknown genomic alterations contributing to drug resistance.
methodsTumor and blood samples from 69 stage IIIB-IV NSCLC patients defined as acquired resistance to first-generation EGFR TKIs (gefitinib, erlotinib or ecotinib) were collected. The cobas
resultsThe overall T790M-positive rate was 52.2% considering all testing methods. Out of 21 samples in which tumor re-biopsy was performed, 14 were T790M positive (66.7%). cMET amplification was identified in three out of seven T790M-negative samples. Exome sequencing in four T790M wildtype/cMET-unamplified samples and paired white blood cells identified a cohort of candidate key mutated genes including BRAF, FGFR1, PAK1, PCNT, PEBP4 and SOX3.
conclusionsEGFR T790M mutation and cMET amplification are main mechanisms leading to EGFR TKI resistance in lung adenocarcinoma. These key mutated genes identified in the present study would need further validation in large number of patients.
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