TABLE 2 .
Top 10 most significantly enriched pathways by pathway enrichment analysis of cancer
| Most significantly enriched pathway (P value) using DE genes from the following disease group(s)a: | ||||
|---|---|---|---|---|
| c-CHB all | c-CHB only | c-CHB and c-CHC overlap | c-CHC all | c-CHC only |
| FXR/RXR activation (1.00E−23) | FXR/RXR activation (2.00E−14) | LXR/RXR activation (1.1E−08) | LXR/RXR activation (4.27E−09) | Pathogenesis of multiple sclerosis (7.94E−05) |
| LPS/IL-1-mediated inhibition of RXR function (2.51E−18) | LPS/IL-1-mediated inhibition of RXR function (2.95E−10) | FXR/RXR activation (2.88E−08) | LPS/IL-1-mediated inhibition of RXR function (1.20E−07) | Cell cycle G1/S checkpoint regulation (3.89E−03) |
| LXR/RXR activation (2.51E−16) | Acute-phase response signaling (3.72E−10) | LPS/IL-1-mediated inhibition of RXR function (5.25E−08) | FXR/RXR activation (8.71E−07) | Protein kinase A signaling (5.50E−03) |
| Acute-phase response signaling (1.58E−12) | LXR/RXR activation (1.02E−07) | Chemokine signaling (1.17E−04) | Complement system (7.41E−05) | Small cell lung cancer signaling (5.62E−03) |
| Blood flow/coagulation system (3.31E−09) | Intrinsic prothrombin activation pathway (6.17E−07) | Aryl hydrocarbon receptor signaling (3.55E−04) | Phosphatidylcholine biosynthesis (3.31E−04) | Cyclins and cell cycle regulation (7.76E−03) |
| Intrinsic prothrombin activation pathway (4.27E−08) | Extrinsic prothrombin activation pathway (6.46E−07) | Fatty acid α-oxidation (6.76E−04) | Hepatic cholestasis (4.07E−04) | RAR activation (8.71E−03) |
| Complement system (6.31E−08) | Phenylalanine degradation (2.34E−06) | Dopamine degradation (7.24E−04) | Aryl hydrocarbon receptor signaling (4.27E−04) | Granulocyte adhesion and diapedesis (8.91E−03) |
| Estrogen biosynthesis (7.94E−08) | Blood flow/coagulation system (6.46E−06) | Atherosclerosis signaling (7.41E−04) | Bile acid biosynthesis, neutral pathway (5.50E−04) | Glioma signaling (1.55E−02) |
| Xenobiotic metabolism signaling (1.02E−07) | Xenobiotic metabolism signaling (2.29E−05) | Complement system (7.76E−04) | Chemokine signaling (6.76E−04) | Type I diabetes mellitus signaling (2.45E−02) |
| Valine degradation (1.2E−07) | Valine degradation (2.63E−05) | Blood flow/coagulation system (1.12E−03) | Blood flow/coagulation system (6.92E−04) | IL-17A signaling in gastric cells (2.57E−02) |
a
Top ten most significantly enriched pathways from Ingenuity Pathway Analysis using either all differentially expressed (DE) genes of a disease group (“all”), DE genes of a disease group with no overlap with any other group (“only”), or DE genes shared between two disease groups (“overlap”). Abbreviations: LPS, lipopolysaccharide; RAR, retinoid acid receptor.