By induction of wt-Apc orβ-catenin silencing in HT29 cells, we observed that several genes in theNotch pathway, including Notch-2, were downregulated.Finally, active Notch signaling was verified in theApcMin/+ mouse modelwhere Hes-1 mRNA levels were found significantlyupregulated in intestinal tumors compared to normal intestinal mucosa.Luciferase assays showed an increased activity for the core and proximalNotch-2 promoter upon co-transfection of HCT116 cellswith high expression recombinant Tcf-4, Lef-1 or β-catenin. This evidence concerns the gene NOTCH2 and intestinal neoplasm.