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Table 1 The 20 most significantly enriched pathways between all primary and metastatic samples.

From: Molecular profiling supports the role of epithelial-to-mesenchymal transition (EMT) in ovarian cancer metastasis

  Functional pathways pValue
1 Cytoskeleton remodeling_TGF, WNT and cytoskeletal remodeling 1.53E-13
2 Cell adhesion_ECM remodeling 1.03E-11
3 Cytoskeleton remodeling_Cytoskeleton remodeling 7.54E-11
4 Development_Regulation of epithelial-to-mesenchymal transition (EMT) 9.43E-11
5 Cell adhesion_Chemokines and adhesion 1.75E-10
6 Oxidative phosphorylation 1.99E-10
7 Development_TGF-beta-dependent induction of EMT via MAPK 2.05E-09
8 DNA damage_Brca1 as a transcription regulator 3.36E-09
9 Cytoskeleton remodeling_Reverse signaling by ephrin B 6.64E-09
10 LRRK2 in neurons in Parkinson’s disease 2.32E-08
11 Apoptosis and survival_BAD phosphorylation 5.22E-08
12 Development_TGF-beta-dependent induction of EMT via RhoA, PI3K and ILK 5.30E-08
13 Cytoskeleton remodeling_Role of PKA in cytoskeleton reorganisation 1.30E-07
14 Transcription_Androgen Receptor nuclear signaling 2.02E-07
15 Immune response_MIF-induced cell adhesion, migration and angiogenesis 3.06E-07
16 Immune response_MIF - the neuroendocrine-macrophage connector 3.06E-07
17 Development_TGF-beta-dependent induction of EMT via SMADs 5.02E-07
18 Cell adhesion_Integrin-mediated cell adhesion and migration 6.77E-07
19 Transport_Clathrin-coated vesicle cycle 7.47E-07
20 Cell adhesion_Role of tetraspanins in the integrin-mediated cell adhesion 1.27E-06
  1. Enriched pathways were computed utilizing the 3,365 significantly differentiated expressed genes (4,389 probe sets) represented in the clustering analysis (Figure 1). Thirteen of the 20 pathways (highlighted in bold) are involved in EMT or EMT-related processes (iCe., cytoskeleton remodeling, cell adhesion, EMT developmental processes, MIF-associated cell adhesion).