摘要：The pathogenesis of bladder cancer is being analyzed at several levels of biological organization, i.e., population groups, individual whole animal, tissue, cell, molecule, etc. Each of these levels provides opportunities for mechanistic studies. Yet the integration of these several levels into a cohesive fabric is incomplete. From a clinical point of view, the following seem of importance to human bladder cancer pathogenesis. The initiation, promotion, and progression of bladder cancer involves several factors acting concurrently or sequentially. These factors appear to be naturally occurring or synthetically created chemicals present in the external environment. Human exposures to these agents may begin in utero , and varying, dynamic qualitative and quantitative exposure patterns continue through developmental and adult life. Apparent latent periods of development of clinical bladder cancer may be as short as one, or as long as 50 years or more. Individuals may exhibit differential susceptibility to vesical carcinogens, perhaps through phenotypic differences in quantitative biotransformation routes. Differences in bladder epithelial cell susceptibilities probably also occur, as well as varying local tissue and generalized resistance to neoplasia formation. Older individuals do not appear to be more resistant to bladder carcinogenesis. A number of animal model systems have been developed for the study of the in vivo , cellular, and molecular pathogenesis of bladder cancer. These models replicate many of the known salient features of human bladder cancer. Through use of appropriate whole animal models in conjunction with investigations of human and animal bladder cells and tissues in culture, controlled mechanistic and quantitative studies of bladder cancer pathogenesis should rapidly develop. Full text Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (1.2M), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References . 201 202 203 204 205 206 207
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