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By R. Doll (auth.), Prof. Dr. rer. nat. Manfred Schwab, Prof. Dr. med. Hartmut M. Rabes, Prof. Dr. med. Klaus Munk, Prof. Dr. med. Hans Peter Hofschneider (eds.)

Different melanoma kinds may end up from a multiplicity of environmental and genetic components. Molecular epidemiology has centred lately on elucidating relationships among specific genetic adjustments and the kind of environmental publicity. a number of genes were pointed out as robust determinants for a few melanoma forms. the unfinished penetrance usually evidenced via mutations of those genes has raised the chance that extra endogenous or exogenous determinants are fascinated about melanoma improvement or suppression. the main target of this ebook is to offer an built-in view of environmental, epidemiological, and genetic determinants that give a contribution to melanoma susceptibility and progression.

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1993; Wang et al. 1994, 1995b; Xiao et al. 1994; Leveillard et al. 1996; Gobert et al. , XPB and XPD: Wang et al. 1996). Cellular context determines whether p53 can induce apoptosis, independent or dependent of its transcription transactivation function and in the absence of RNA and protein synthesis (Wang et al. 1996; Caelles et al. 1994; Haupt et al. 1995; Wagner et al. 1994; Del Sal et al. 1995; Sakamuro et al. 1995). Interestingly, cycloheximide, an inhibitor of protein synthesis, can induce apoptosis (Harris et al.

Benzo[a)pyrene (BP), in tobacco smoke cause p53 hotspot mutations at codons 157, 248 and 273 in human lung carcinogenesis Strength of association Consisten

Recent Results in Cancer Research, Vol. 154 © Springer-Verlag Berlin· Heidelberg 1998 Breast. lung, other Breast. other lung, other Uver. lung, breast cervical. other Physiologic Hormonal Metabolic Immunologic, chronic disease. nutritional Age Gender Preexisting impairment Altered metabolism (substrate: PAH) Altered metabolism

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