At the invasion front of well-differentiated colorectal adenocarcinomas, the oncogene β-catenin is found in the nuclear compartment of tumor cells. Under these conditions, β-catenin can function as a transcription factor and thus activate target genes. One of these target genes, cyclin D 1, is known to induce proliferation. However, invasion front of well-differentiated colorectal adenocarcinomas are known to be zones of low proliferation and express the cell cycle inhibitor p16 INK4A. Therefore, we investigated the expression profiles of nuclear β-catenin, cyclin D 1, p16 INK4A, and the Ki-67 antigen, a marker for proliferation, in serial sections of well-differentiated colorectal adenocarcinomas. Invasion fronts with nuclear β-catenin were compared with areas from central parts of the tumors without nuclear β-catenin, for the expression of cyclin D 1, p16 INK4A, and Ki-67. It was observed that expression of nuclear β-catenin, cyclin D 1, and p16 INK4A at the invasion front are significantly correlated. Such areas exhibit low Ki-67 expression indicating a low rate of proliferation. Thus, in colorectal carcinogenesis the function of β-catenin and its target gene cyclin D 1 does not appear to be the induction of tumor cell proliferation. In particular, the function of cyclin D 1 should be reconsidered in view of these observations.