Carcinogenesis and genotoxicity

摘要: R. Marchan Leibniz Research Centre for Working Environment and Human Factors (IfADo), Ardey-strasse 67, 44139 Dortmund, Germany E-mail: marchan@ifado.de, Telephone: +49 231-1084-213, Fax: 231-1084-403 Carcinogenesis (Table 1A) genotoxicity 1B) are two of the most popular topics published in our partner journal Archives Toxicology. A particular highlight was an article 2008 by Kohle et al. on hepatocarcinogenesis humans rodents. It is fairly well-accepted that major interspecies differences between human rodents can compro-mise extrapolation hepatocarcinogenesis. In their publication, (2008) addressed topic concluded a relatively high degree similarity exists rodent genotoxic-initiating carcinogens. However, remarkable species have been observed nongenotoxic tumor pro-moters. colleagues differentiated modes action: (1) chronic cyto-toxicity leading to replacement proliferation, which often occurs both rodents, (2) sustained activation orphan receptors such as CAR, PPAR alpha Ah recep-tor. report these mechanisms much more relevant than hu-mans may explain considerable part differences. second novel classification carcinogens SCOEL (Scientific Com-mittee Occupational Exposure Limits) reported Bolt Huici-Montagud (2008), where classified according possibility establish either “practical” or “true” thresholds. Class represents non-threshold genotoxic linear model appears appropriate. B comprises existence threshold cannot be sufficiently supported. Therefore because scien-tific uncertainty, liner should used. C includes with practical (as described Hengstler al., 2003) exposure limits based established NOAEL. D non-genotoxic non-DNA-reactive car-cinogens “perfect” established. An overview publications carcinogenesis given Table 1.