By H.-J. Senn, U. Kapp

This quantity comprises the most court cases of the fourth foreign convention on "Cancer Prevention 2006," which used to be held in the course of February 16–18, 2006, in St. Gallen, Switzerland. Written through foreign specialists within the box, the publication contains a finished replace at the most up-to-date 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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We thank Birgit Jäger, Reinhard Gliniorz, Otto Zelezny and Peter Waas for skilled technical assistance. We sincerely acknowledge the contributions by our collaborators: L. Edler, Biostatistik, DKFZ; P. Drings, H. Dienemann, K. W. Kayser, V Schulz, Thoraxklinik Heidelberg-Rohrbach; A. C. von Brevern, Axaron Bioscience AG, Heidelberg, A. Bürkle, Abtl. Molekulare Toxikologie, Universität Konstanz; H. Becher, Abteilung Tropenhygiene und öffentl. Gesundheitswesen, Universität Heidelberg; H. Ramroth, Abteilung Klinische Epidemiologie, DKFZ; A.

01) when all lung cancer cases were compared with controls. 029) (Dally et al. 2002) (see Fig. 1). Since 1997, controversial results have been published regarding the MPO-463A allele and its impact on lung cancer. This seems to be mainly due to differing proportions of histological types of lung cancer as well as differences in the number of never-smokers among cases and controls in several studies. The MPO genotype frequencies may also differ in nonmalignant lung diseases. As lung tumor development is frequently preceded by chronic inflammation of the lung (Mayne et al.

For NAT2, carriers of at least one wild type allele were considered fast acetylators. Multivariate logistic regression analyses were performed taking into account levels of smoking, age, gender, and occupational exposure (Wikman et al. 2001). 16) was found but could not be detected for SCC or the total case group (see Fig. 2). 81), which was higher than that observed for NAT1 and AC alone (Wikman et al. 2001). This data clearly shows the importance of separating different histological lung tumor subtypes in studies on genetic susceptibility factors and implicates the NAT1*10 allele as a risk factor for adenocarcinoma.

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