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By H.-J. Senn, U. Kapp

This quantity comprises the most court cases of the fourth foreign convention on "Cancer Prevention 2006," which was once held in the course of February 16–18, 2006, in St. Gallen, Switzerland. Written by way of foreign specialists within the box, the booklet contains a entire replace at the newest advancements within the upsurging fields of molecular biology and melanoma genetics and their interactions with medical epidemiology and melanoma prevention at a variety of levels.

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Cancer Prevention

This quantity includes the most lawsuits of the fourth foreign convention on "Cancer Prevention 2006," which was once held in the course of February 16–18, 2006, in St. Gallen, Switzerland. Written by way of foreign specialists within the box, the booklet contains a entire replace at the newest advancements within the upsurging fields of molecular biology and melanoma genetics and their interactions with medical epidemiology and melanoma prevention at numerous degrees.

Extra resources for Cancer Prevention

Example text

The best recognized examples are genetic polymorphisms of drug-metabolizing enzymes, which affect 30% of all drugs (Eichelbaum et al. 2006), but inherited variations in DNA repair, in drug transporter genes and other drug target genes also likely contribute to the variability in the outcome of cancer treatment (Efferth and Volm 2005; Lee et al. 2005). Given the number and variability in expression of carcinogen-metabolizing and DNA repair genes and the complexity of human carcinogen exposures, assessment of a single polymorphic enzyme (genotype) for risk prediction or therapy outcome is not sufficient.

2004). In an ongoing pharmacogenetic study, the influence of certain SNPs and haplotypes on chemotherapy response outcome and survival in patients with primary lung cancer is being investigated. These concern enzymes that metabolize and transport anticancer agents used in lung cancer treatment. In addition, the influence of repair enzymes, especially those that play a critical role in platinum resistance is being analyzed. All patients receive a first-line chemotherapy. Chemotherapy response is assessed after the second cycle to detect mainly host factor-related 30 mechanisms of resistance and to exclude, as far as possible, acquired mechanisms of resistance in the tumor developed during treatment.

After adjustment for age, gender, and smoking status, the cases versus controls had a more than twofold reduction in DNA repair capacity and a fourfold increase in mutagen sensitivity. Bleomycin sensitivity and DNA repair capacity were found to be independent susceptibility markers for non-small cell lung cancer. Our results revealed the comet assay to be a sensitive and fast tool that can be applied both to native and cryopreserved peripheral blood lymphocytes. It is suitable to determine individual mutagen sensitivity and DNA repair capacity in whole cells, thus allowing the assessment of complex phenotypes of integrated response to DNA damage.

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