The study ofneoplasia in aquatic animals has largely focused onmorphology and epizootiology. Correlations have been sought between prevalences of specific lesion types and significant biological and environmental variables as potential etiological factors. These factors have included age, gender, and exposure to chemical contaminants and infectious agents, as well as predisposing genetic characteristics. Experiments have shown a number of chemicals to be hepatocarcinogens in fish. These include aflatoxin in rainbow trout and nitroso-compounds, azo compounds, methylazoxymethanol acetate, polynuclear aromatic hydrocarbons, and aromatic amines in trout, medaka, guppy, zebra danio, mangrove rivulus, sheepshead minnow, and topminnow. Furthermore, the carcinogenicity of extracts derived from chemically contaminated sediments has been demonstrated in the rainbow trout and the brown bullhead, and putatively preneoplastic focal hepatic lesions have been induced in English sole by exposure to similar sediment extracts. However, we know less of the significance of polychlorinated biphenyls (PCBs), chlorinated pesticides, and other nongenotoxic agents as promoters of the hepatocarcinogenic

process in laboratory and feral species of fish. In this context, we discuss the mechanisms of chemical carcinogenesis in fish species exposed to environmentally important chemicals and the application of current and more sophisticated methods to elucidate these mechanisms.