Abstract
Calcium has been hypothesized as being a regulator of cell proliferation in the colon. Epidemiologic studies suggest that ingestion of higher levels of dietary calcium are related to a decreased risk for colon cancer. Short term studies in vitro and in vivo of the proliferative behavior of human and animal colon mucosa verify that calcium does modulate proliferative response. Preliminary clinical studies suggest that the hyperproliferative mucosa of patients at high risk for colon cancer, based on proliferation analysis of biopsied mucosa, became decidedly less proliferative when the subjects were given oral calcium. Our studies address the molecular mechanisms by which calcium controls mucosal proliferation and the ways in which tumor cells circumvent this regulation.