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. 2012 Mar 15;109(16):5934–5941. doi: 10.1073/pnas.1202490109

Table 1.

Signaling pathways enriched for CCGs

Signaling pathways and cellular processes Percent tumor Number CCG (GKC method) P value Number CCG (gCIS method) P value Representative genes Analysis platform
Molecular mechanisms of cancer 100 13 2.25E-06 35 8.79E-07 Crebbp, Gsk3b, Mll3, Pten, and Nsd1 IPA
GO:0016568−  chromatin modification 100 14 3.52E-05 34 3.26E-08 Kdm6a, Mll3, Mll5, Myst3, and Nsd1 DAVID
TGF-β 90 7 3.46E-06 16 1.5E-06 Acvr2a, Crebbp, Smad2, Smad4, and Smurf2 IPA
RAR activation 90 9 5.72E-06 21 1.27E-05 Ncor1, Nsd1, Pdpk1, and Pik3r1 IPA
HGF signaling 90 7 1.12E-05 21 7.69E-09 Atf2, Dock1, Grb2, Ptk2, Ptpn11, and Rap1a IPA
ERK/MAPK 90 8 8.89E-05 19 2.84E-04 Grb2, Mapk1, Pak1, and Ptk2 IPA
Tight junction signaling 90 8 1.25E-03 17 9.91E-05 Ash1l, Ctnna1, Inadl, Magi1, and Magi2 KEGG
GO:0003682− chromatin binding 90 9 6.6E-03 22 3.04E-05 Adnp, Arid4b, Gata6, Mbd1, and Ncoa1 DAVID
PI3K/Akt 86 7 3.72E-05 15 2.14E-04 Mapk1, Pdpki, Pik3ca, Pten, and Rps6kb1 IPA
Integrin 86 8 1.48E-04 23 1.39E-05 Arhgap5, Itgb1, Ptk2, and Rapgef1 IPA
Ephrin receptor 86 7 3.7E-04 21 1.51E-05 Abi1, Cdc42, Epha6, Gnaq, and Gna14 IPA
Rac Signaling 86 5 1.25E-03 15 5.29E-05 Cdc42, Iqgap1, Iqgap2, Map3k1, and Pak1 IPA
Formation of filaments 81 10 6.75E-05 32 4.41E-05 Akap13, Atxn2, Ctnnd1, and Fhit IPA
Wnt/β-catenin 76 5 1.02E-02 18 3.17E-04 Csnk1d, Gnaq, Gsk3β, EP300, and Ppp2r5e IPA
Adherens junction 76 5 1.6E-02 15 7.42E-06 Actn1, Cdh1, Crebbp, Ctnna1, and Ctnnd1 KEGG

Analysis of CCGs using IPA, DAVID, and KEGG revealed several canonical signaling pathways and processes enriched for CCGs from SB-driven pancreatic tumors. Percent tumor is the proportion of tumors that had a mutation in at least one CCG found within the pathway; 48 GKC CCGs and 174 gCCGs were significantly enriched in canonical pathways identified by IPA. P values for pathway enrichment were adjusted for multiple testing using the Benjamini–Hochberg method for control of the false discovery rate.

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