Exploring the Cause of Survival Disparities in EGFR-Mutated Lung Cancer Subtypes: Unraveling Distinctive Genomic and Phenotypic Features of 19Del and L858R Mutation Subtypes
摘要
Different efficacy of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI) has been observed between lung cancer patients with 19 exon deletion (19Del) and with L858R mutation. We investigate the multi-omics information from the TCGA Lung adenocarcinoma (LUAD) dataset and validate it using the GEO (GSE190139, GSE147377) and MSK datasets. Somatic loss-of-function alteration of RBM10 and altered Immune infiltration profile correlated with L858R decreased survival. Meanwhile, 9p21.3 loss, CDKN2B methylation, and increased cell cycle-related gene expression are differential characteristics in the L858R mutation group. Comprehensive genomic and phenotypic analysis of the EGFR-mutated lung cancer subtypes reveals distinctive features of each subtype, laying the groundwork for subtype-specific treatment and care options for lung cancer patients.