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In lung adenocarcinoma, the mutational spectrum is dominated by  EGFR  and  KRAS  mutations. Improved knowledge about genomic and transcriptional alterations in and between mutation-defined subgroups may identify genes involved in disease development or progression.    Methods  Genomic profiles from 457 adenocarcinomas, including 113  EGFR -mutated, 134  KRAS -mutated and 210  EGFR  and  KRAS -wild type tumors (EGFRwt/KRASwt), and gene expression profiles from 914 adenocarcinomas, including 309  EGFR -mutated, 192  KRAS -mutated, and 413 EGFRwt/KRASwt tumors, were assembled from different repositories. Genomic and transcriptional differences between the three mutational groups were analyzed by both supervised and unsupervised methods.    Results    EGFR -mutated adenocarcinomas displayed a larger number of copy number alterations and recurrent amplifications, a higher fraction of total loss-of-heterozygosity, higher genomic complexity, and a more distinct expression pattern than  EGFR -wild type adenocarcinomas. Several of these differences were also consistent when the three mutational groups were stratified by stage, gender and smoking status. Specific copy number alterations were associated with mutation status, predominantly including regions of gain with the highest frequency in  EGFR -mutated tumors. Differential regions included both large and small regions of gain on 1p, 5q34-q35.3, 7p, 7q11.21, 12p12.1, 16p, and 21q, and losses on 6q16.3-q21, 8p, and 9p, with 20-40% frequency differences between the mutational groups. Supervised gene expression analyses identified 96 consistently differentially expressed genes between the mutational groups, and together with unsupervised analyses these analyses highlighted the difficulty in broadly resolving the three mutational groups into distinct transcriptional entities.    Conclusions  We provide a comprehensive overview of the genomic and transcriptional landscape in lung adenocarcinoma stratified by  EGFR  and  KRAS  mutations. Our analyses suggest that the overall genomic and transcriptional landscape of lung adenocarcinoma is affected, but only to a minor extent, by  EGFR  and  KRAS  mutation status.

Genomic and Transcriptional Alterations in Lung Adenocarcinoma in Relation to EGFR and KRAS Mutation Status