Supplementary Figure 5 from SIRT1 Pathway Dysregulation in the Smoke-Exposed Airway Epithelium and Lung Tumor Tissue

PDF file, 72K, SIRT1 and PI3K pathway activation in airway epithelial cells from current and formers smokers with and without lung cancer. CEL files from the training and test set samples in GSE4115 (n=129 samples, n=29 current smokers with lung cancer, n=22 current smokers without lung cancer, n=31 former smokers with lung cancer, n=26 former smokers without lung cancer) were processed as described in the methods. The pathway signature for PI3K was re-derived using the methods described above using a compendium of oncogenic signatures including BCAT, E2F3, MYC, p63, RAS, and SRC (GSE3151 and GSE12815). PI3K pathway activation probabilities for each sample were computed using the same methodology described for SIRT1. A. There is no significant difference in SIRT1 pathway activation between patients with and without lung cancer. SIRT1 is significantly activated in current smokers compared to former smokers (p<0.001). B. PI3K is significantly activated in patients with lung cancer (p<0.001).