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Table 2 Top 20 pathways in the 500 signatures of ER-positive and ER-negative tumors evaluated by Global Test

From: Pathway analysis of gene signatures predicting metastasis of node-negative primary breast cancer

Pathways GO_ID P Frequency
ER-positive tumors    
   Apoptosis 6915 3.06E-7 250
   Regulation of cell cycle 74 2.46E-5 203
   Protein amino acid phosphorylation 6468 2.48E-5 114
   Cytokinesis 910 6.13E-5 165
   Cell motility 6928 0.00015 93
   Cell cycle 7049 0.00028 138
   Cell surface receptor-linked signal transd. 7166 0.00033 172
   Mitosis 7067 0.00036 256
   Intracellular protein transport 6886 0.00054 141
   Mitotic chromosome segregation 70 0.00057 98
   Ubiquitin-dependent protein catabolism 6511 0.00074 158
   DNA repair 6281 0.00079 156
   Induction of apoptosis 6917 0.00083 115
   Immune response 6955 0.00094 167
   Protein biosynthesis 6412 0.0010 145
   DNA replication 6260 0.0015 92
   Oncogenesis 7048 0.0020 228
   Metabolism 8152 0.0021 83
   Cellular defense response 6968 0.0025 131
   Chemotaxis 6935 0.0027 89
ER-negative tumors    
   Regulation of cell growth 1558 0.00012 136
   Regul. of G-coupled receptor signaling 8277 0.00013 153
   Skeletal development 1501 0.00024 160
   Protein amino acid phosphorylation 6468 0.0051 151
   Cell adhesion 7155 0.0065 110
   Carbohydrate metabolism 5975 0.0066 86
   Nuclear mRNA splicing, via spliceosome 398 0.0067 203
   Signal transduction 7165 0.0078 160
   Cation transport 6812 0.0098 160
   Calciumion transport 6816 0.010 93
   Protein modification 6464 0.011 132
   Intracellular signaling cascade 7242 0.012 135
   mRNA processing 6397 0.012 81
   RNA splicing 8380 0.014 192
   Endocytosis 6897 0.026 166
   Regul. of transcription from PolII promoter 6357 0.031 109
   Regulation of cell cycle 74 0.043 88
   Protein complex assembly 6461 0.048 183
   Protein biosynthesis 6412 0.063 99
   Cell cycle 7049 0.084 72
  1. Each of the top 20 over-represented pathways that have the highest frequencies in the 500 signatures of ER-positive and ER-negative tumors were subjected to Global Test program [12, 14]. The Global Test examines the association of a group of genes as a whole to a specific clinical parameter, in this case DMFS, and generates an asymptotic theory p value for the pathway. The pathways are ranked by their p value in the respective ER-subgroup of tumors.