There is ongoing controversy over whether mucosal hyperproliferation is involved in colorectal carcinogenesis. The hypothesis that was originally offered to explain the transition from normal mucosa to a benign epithelial neoplasm in which the tumor cells form glands or gland-like structures used a three stage process. At stage I, the proliferative compartment of the colorectal crypt, which is usually confined to the lower one-third of the crypt, extends upward and envelops the entire crypt. At stage II, the maximum of the proliferative compartment shifts to the upper portion of the crypt, and, at stage III, the total number of replicating cells in the crypt rises, leading to mucosal hyperproliferation and subsequently -- due to the influence of co-factors -- to a tumor. However, in patients with sporadic colorectal cancer, findings are debatable, and the scientific literature is divided into reports supporting or contesting the importance of the stage III defect for adenoma and carcinoma formation.
One possible explanation for this discrepancy in patients with sporadic colorectal cancer might be found in the techniques used to evaluate mucosal proliferation. Most of these methods are applied in vitro and are cytostatic, i.e., providing an estimate of only the fraction of proliferating cells in a particular phase of the cell cycle at a given moment. This information can be misleading, since it uses no measure of time (length of the cell cycle). The duration of the cell cy
Contact: Donna Krupa
American Physiological Society