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ABSTRACT: Background
When considering therapies for lung adenocarcinoma (LUAD) patients, the carcinogenic mechanisms of smokers are believed to differ from those who have never smoked. The rising trend in the proportion of nonsmokers in LUAD urgently requires the understanding of such differences at a molecular level for the development of precision medicine.Methods
Three independent LUAD tumor sample sets-TCGA, SPORE and EDRN-were used. Genome patterns of expression (GE), copy number variation (CNV) and methylation (ME) were reviewed to discover the differences between them for both smokers and nonsmokers. Tobacco-related signature genes distinguishing these two groups of LUAD were identified using the GE, ME and CNV values of the whole genome. To do this, a novel iterative multi-st
SUBMITTER: Dong YM
PROVIDER: S-EPMC6995662 | biostudies-literature | 2020
REPOSITORIES: biostudies-literature