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genetic disorder showed the higher number of associated molecules (P < 10 -4 ). Cell cycle,cellular assembly and organization, as well as cellular growth and proliferation were themajor functions associated with dataset (P < 10 -3 ) (Figure 3B).Sixty-one canonical pathways were found to be significantly associated withmodulators, even though only 37 pathways were associated with the selected genes (Figure3A). Eight out of 14 genes were associated with different canonical pathways including theintrinsic prothrombin activation pathway (COL3A1), FGF signaling (FGFR1), ERK/MAPKsignaling (HSPB7), VDR/RXR activation (IGFBP5), mTOR signaling (RHOH), FAKsignaling (TNS1), and G-Protein coupled receptor signaling (CALCRL, GPR4) (Figure 4A).The canonical pathway hepatic fibrosis/hepatic stellate cell activation revealed theinvolvement of COL3A1, FGFR1, and IGFBP5 genes (P < 0.01), showing similarity tobiological pathways already described in ULs (Figure 3C).DISCUSSIONBased on in silico approaches integrating genomic and transcriptomic profiles, thepresent study has revealed candidate genes and molecular pathways associated with ULspathogenesis.Array CGH and gene expression microarray data of 51 ULs samples from 34 patientsrevealed 1192 genomic imbalances and 3325 up- or down-regulated transcripts, respectively.The integrative analysis using CONEXIC [17] identified 75 modulators that explain the 3325differentially expressed genes. The modulators were distributed on 25 chromosomal regions,seven of them were previously described by HR-CGH or array CGH studies in ULs,including 1p36.13, 4p14, 7q22.1, 11p15.5, 14q13.2, 19q13.32 and 19q13.33 [30, 31, 15, 11,32]. Furthermore, it was also verified new genomic imbalances involved in ULs mapped on1q41, 2q32.1, 2q32.2, 2q35, 5q31.2, 5q35.3, 8p12, 8q24.3, 10p15.3, 10q21.3, 11q13.2,10