Author(s) :

Leyla Bac.

Volume/Issue :

Abstract :

Smoking is a major contributor to lung adenocarcinoma, yet its specific gene expression signature remains unclear. This study, with a sample size of n=107, examined gene expression differences across current, former, and never smokers, as well as tumor and non-tumor lung samples, to better define smoking’s molecular impact. Ordinary least squares regression and ANOVA were applied to the microarray GSE10072 data, followed by false discovery rate correction using the Benjamini–Hochberg method with a statistical threshold of q<0.05. The analysis identified many differentially expressed genes for each comparison: 10562 genes for tumor vs non-tumor, 627 genes for current vs never smokers, and 18 genes for former vs never smokers. Specific genes of interest include CYP1B1, upregulated by 110.8-148.8% across 3 probes in current smokers, and ADARB1, downregulated by 36.4%, 23.3%, and 73.2% in current smokers, former smokers, and tumor samples, respectively. These genes, implicated in pathways such as AHR-CYP and PI3K/AKT signaling, highlight potential mechanistic links between smoking exposure and lung cancer development. The results suggest that smoking leaves distinct and lasting molecular signatures that may contribute to tumor progression, offering potential targets for improved therapeutic strategies.