ABSTRACT
In an overview of chemical carcinogenesis, Miller l described historical events that provided a foundation for modem research on chemical carcinogenesis. Among the important landmarks were the observations of scrotal skin cancer in chimney sweeps by Pott,2 work by Japanese researchers demonstrating induction of skin cancer by coal tar,3-5 isolation ofbenzo(a)pyrene (BaP) from coal tar,6 and the description of initiation and promotion stages of skin cancer with tar and BaP.7-1O In addition to these studies, the recognition and demonstration ofcovalent binding of chemicals to macromolecules, especially DNA, provided impetus for evaluating the role of such interactions in the process of carcinogenesis. I 1-13 In the years that followed, numerous adducts formed by a variety of chemical agents were described. 14--16
The study of carcinogenesis in fish has similar landmark studies. Although there were reports of tumors in the early literature,17 the first epizootic of liver neoplasia in wild fish was reported in 1964 by Dawe et al. 18 In that report, the authors suggested the use of bottom-feeding fish to detect environmental carcinogens. Since then, the number of reports of epizootics of fish tumors in North America has been ever increasing, with many of them describing liver tumors in bottom-dwelling fish from areas with high levels of environmental pollutants.17
Around the same time as the first description of liver tumors in wild fish, worldwide occurrences of liver tumors in hatchery-raised rainbow trout were described. 19-22 Subsequent research pinpointed the cause of the cancer as a potent hepatocarcinogen, Aflatoxin B1 (AFB 1), which had contaminated the vegetable protein component of the commercial diet being fed to the trout.23-25 The discovery of the sensitivity of rainbow trout to chemically induced liver tumors thus led to the development of a rainbow trout laboratory model for studying chemical carcinogenesis and encouraged the development of other fish model systems.26-33
