A rationale for the loss of growth control during experimental bladder carcinogenesis.

A rationale is presented which provides an explanation for the loss of growth control which is associated with the early phase of experimentally-induced bladder cancer. Two early events which occur in the urothelium following exposure to carcinogen, the focal loss of alkaline phosphatase activity and the initiation of cell proliferation, are both proposed to be the result of a defect in the interaction between glucocorticoid hormone and urothelium. The possible causes for this defect are discussed in terms of a defect in, or an interference with, the glucocorticoid-receptor mechanism.