Cancer Prevention by H.-J. Senn, U. Kapp

By H.-J. Senn, U. Kapp

This quantity comprises the most lawsuits of the fourth overseas convention on "Cancer Prevention 2006," which used to be held in the course of February 16–18, 2006, in St. Gallen, Switzerland. Written via foreign specialists within the box, the publication includes a finished replace at the most modern advancements within the upsurging fields of molecular biology and melanoma genetics and their interactions with medical epidemiology and melanoma prevention at numerous levels.

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No genotype-dependent increase in OR was found for those smoking less than 20 pack-years or for nonexposed individuals (see also Butkiewicz et al. 2004) between different pathways are required. Our results on combined genotypes indicate that lung cancer risk is considerably enhanced by specific combinations of variant alleles. The interaction of several (or many) variant repair proteins, each with only slightly reduced functional activity, may be necessary to significantly decrease DNA repair activity and to increase cancer risk.

In addition, the histogenesis of SCLC is completely different from that of NSCLC because it morphologically and immunohistochemically belongs to the neuroendocrine tumors (Kayser 1992; Brambilla et al. 2005). The MPO-463 polymorphism is a good example, showing that separate analysis of different histological types of lung cancer is important in risk assessment. MPO-463 has functional significance for metabolism and DNA binding 21 of carcinogens present in tobacco smoke. We conducted a case–control study with 625 eversmoking lung cancer patients that included 228 adenocarcinomas, 224 SCC and 135 SCLC, as well as 340 ever-smoking hospital-based controls.

Genes and their products that are involved in cancer susceptibility may also modulate therapeutic outcome of anti-cancer drugs (Spitz et al. 2005). Interindividual differences in therapy response are consistently observed with most chemotherapeutic agents or regimens. Pharmacogenetic investigations are trying to link inher- Helmut Bartsch et al. ited genetic differences to the therapy response by specific drugs. The best recognized examples are genetic polymorphisms of drug-metabolizing enzymes, which affect 30% of all drugs (Eichelbaum et al.

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