ECNIS-sponsored workshop on biomarkers of exposure and cancer risk: DNA damage and DNA adduct detection and 6th GUM-32P-postlabelling workshop, German Cancer Research Center, Heidelberg, Germany, 29-30 September 2006.
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AbstractOf all the chemicals classified as carcinogenic to humans by the International Agency for Research on Cancer (IARC), 90% exert their biological effects through binding of their metabolically activated intermediates to DNA forming covalent DNA adducts. As a consequence DNA adducts are generally considered to be causative and directly related to tumour formation. DNA adduct analyses reflect tissue-specific rates of adduct formation and removal, which depend on carcinogen uptake, metabolic activation, DNA repair, adduct instability and tissue turnover and are thus useful markers of carcinogen exposure. The measurement of carcinogen-DNA adduct levels is central to the understanding of chemical carcinogenesis both in animals and humans to determine molecular mechanisms and exposure. Sensitive methods for DNA adduct analysis used to date are based on (32)P-post-labelling, immunoassay, mass spectrometry and laser-induced fluorescence. The aim of this workshop held over 2 days (29-30 September 2006) at the German Cancer Research Center (DKFZ) in Heidelberg, Germany, was to discuss methodological improvements of DNA adduct detection with emphasis on the (32)P-post-labelling procedure as well as new findings achieved by applying the methods to studies on understanding human cancer mechanisms and to elucidate the relationship between adduct formation and human cancer risk.
CitationMutagenesis 2007, 22 (1):83-8.
PublisherOxford University Press
SponsorsThe meeting was sponsored by the Environmental Cancer Risk, Nutrition and Individual Susceptibility (ECNIS) EU Network of Excellence, the German Environmental Mutagen Society (GUM) and the German Cancer Research Center (DKFZ). We are most grateful for the financial support of Novartis Pharma AG (Basel, Switzlerland), Merck KGaA (Darmstadt, Germany), Roche Diagnostics GmbH (Mannheim, Germany), Schering AG (Berlin, Germany), Altana Pharma AG (Hamburg, Germany), BASF AG (Ludwigshafen, Germany) and Boehringer-Ingelheim GmbH (Ingelheim, Germany). We thank the United Kingdom Environmental Mutagen Society (UKEMS) for providing student travel grants. The authors also wish to acknowledge the contribution made by participants to the preparation of this article through the provision of abstracts to the workshop. All oral and poster abstracts have been published online by the European Journal of Molecular and Genetic Toxicology.