TABLE 4.
Differentially enriched pathways (up‐ or downregulated) from all three omics datasets between each omics‐associated cluster (OAC) versus the rest.
| Omics‐associated clusters (OAC) | Pathways identified by all three omics datasets |
|---|---|
| OAC1 | Cell adhesion; Plasmin signalling |
| Eosinophil adhesion and transendothelial migration in asthma | |
| OAC2 | Development Regulation of endothelial progenitor cell differentiation from adult stem cells |
| Development Regulation of epithelial‐to‐mesenchymal transition (EMT) | |
| Eosinophil adhesion and transendothelial migration in asthma | |
| Inhibition of neutrophil migration by proresolving lipid mediators in COPD | |
| Nociception Nociceptin receptor signalling | |
| Prolactin/ JAK2 signalling in breast cancer | |
| Proteases and EGFR‐induced mucin synthesis in normal and asthmatic epithelium | |
| Role of cell adhesion in vaso‐occlusion in Sickle cell disease | |
| Role of integrins in eosinophil degranulation in asthma | |
| Role of platelets in allograft rejection | |
| Role of platelets in the initiation of in‐stent restenosis | |
| OAC3 | Role of IL‐23/ T17 pathogenic axis in psoriasis |
| OAC4 | None |
| OAC5 | Development Keratinocyte differentiation |
| ErbB2‐induced breast cancer cell invasion | |
| Immune response IL‐3 signalling via ERK and PI3K |