The fecal ${eta}-glucuronidase$ activity of patients with colon cancer and healthy controls were measured to determine the relationship between the fluctuation of intestinal bacterial ${eta}-glucuronidase$ and colon cancer. The fecal ${eta}-glucuronidase$ activity of patients with colon cancer was 1.7 times higher than that of the healthy controls. However, when these fecal specimens were sonicated, the enzyme activity of patients with colon cancer was 12.1 times higher than that of the healthy controls. The fecal ${eta}-glucuronidase$ activity of human Intestinal bacteria was drastically induced by its substrate or the bile secreted after a subcutaneous injection of 1,2-dimethylhydrazine (DMH) and benzo[a]pyrene into rats. DMH-and benzo[a]pyrene-treated biles induced ${eta}-glucuronidase$ activity in the human intestinal microflora by approximately 1.5- and 2.3-fold, respectively. They also induced ${eta}-glucuronidase$ in E. coli HGU-3, which is a ${eta}-glucuronidase$-producing bacterium from the human intestine. D-saccharic acid 1,4-lactone similarly inhibited fecal ${eta}-glucuronidase$ in several patients with colon cancer in addition to the healthy controls. This suggests that potent ${eta}-glucuronidase$ activity is a prime factor in the etiology of colon cancer.