Table 1b. Reduction of the candidate gene list from Table 1a after additional filtering using GCRMA normalized data

Table 2. Genes mutated in colon cancer cell lines identified using GINI

Table 1a. Candidate genes for sequencing in LS180 cells

Table 1. Genes Significantly Dysregulated in Early HCC Compared With Dysplatic Nodules; 5 genes were up-regulated in cancer including TERT  GPC3  gankyrin (PSMD10)  survivin (BIRC5)  and TOP2A  and 7 were down-regulated including LYVE1 (XLKD1)  E-cadherin (CDH1)  IGFBP3  PDGFRA  TGFA  cyclin D1 (CCND1)  and HGF

Table 4. Validation of the 5 Genes in an Independent Set of 29 Samples

Table 2a. Top-35 discriminatory genes in HCC with and without PVI; 12 genes up-regulated in HCCs with PVI in comparison with HCCs without PVI

Table 2b. Top-35 discriminatory genes in HCC with and without PVI; 23 genes down-regulated in HCCs with PVI in comparison with HCCs without PVI

SuppTable1. The Cluster 1 list of 33 genes

Table S3. Genes 51?180 of the gene signature of EGFR TKI sensitivity

Table 2: Genes 1?50 of the 180-gene signature of EGFR TKI sensitivity

Supplementary Table 1. Induced (m) and suppressed (k) genes in MCF7 and MDAMB-231 cells after exposure to docetaxel

Table 2a. Microarray assessment of neuroendocrine cell?specific genes in normal nonsmokers  normal smokers  smokers with early COPD  and smokers with established COPD

SuppTable 4: Genes differentially expressed in the small airway epithelium of 10 healthy smokers vs 12 healthy non-smokers

SuppTable 6: Comparison of HG-U133 2.0 vs. HG-U133A results

Table 2. Examples of genes differentially expressed in the small airway epithelium in nonsmokers and smokers in functional categories that are relevant for the pathogenesis of COPD

SuppTable 2: Genes differentially expressed in the small airway epithelium of 6 healthy smokers vs 5 healthy non-smokers

SuppTable 5: Examples of genes differentially expressed in the small airway epithelium of 10 smokers vs 12 non-smokers  in functional categories that are relevant for the pathogenesis of COPD