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Carcinogenesis Advance Access originally published online on October 26, 2005
Carcinogenesis 2006 27(3):606-609; doi:10.1093/carcin/bgi248
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Carcinogenesis vol.27 no.3 © Oxford University Press 2005; all rights reserved.

Association of the CASP10 V410I variant with reduced familial breast cancer risk and interaction with the CASP8 D302H variant

Bernd Frank 1, *, Kari Hemminki 1, 2, Barbara Wappenschmidt 3, 4, Alfons Meindl 5, Rüdiger Klaes 6, Rita K. Schmutzler 3, 4, Peter Bugert 7, Michael Untch 8, Claus R. Bartram 6 and Barbara Burwinkel 1

1 Division of Molecular Genetic Epidemiology, German Cancer Research Center, Heidelberg, Germany, 2 Department of Biosciences at Novum, Karolinska Institute, Huddinge, Sweden, 3 Division of Molecular Gynaeco-Oncology, Department of Gynaecology and Obstetrics, Clinical Center University of Cologne, Germany, 4 Center of Molecular Medicine Cologne (CMMC), University Hospital of Cologne, Germany, 5 Department of Gynaecology and Obstetrics, Klinikum rechts der Isar at the Technical University, Munich, Germany, 6 Institute of Human Genetics, University of Heidelberg, Heidelberg, Germany, 7 Institute of Transfusion Medicine and Immunology, Red Cross Blood Service of Baden-Württemberg-Hessia, University of Heidelberg, Faculty of Clinical Medicine, Mannheim, Germany and 8 Department of Gynaecology and Obstetrics at the Ludwig-Maximilians-University, Munich, Germany

* To whom correspondence should be addressed. Tel: +49 6221 421802; Fax: +49 6221 421810; E-mail: b.frank{at}dkfz.de

Dysregulation of apoptosis plays a crucial role in carcinogenesis. As part of death receptor- and mitochondrion-mediated apoptosis, the homologues caspases 10 and 8 may act as low-penetrance breast cancer (BC) susceptibility genes. In death receptor-mediated apoptosis, engagement of death receptors by their ligands involves the assembly of the death-inducing signalling complex (DISC). In mitochondrion-mediated apoptosis, the release of cytochrome c into the cytosol results in apoptosome formation. Recruitment of both caspases 10 and 8 (CASP10 and CASP8, respectively) to DISC and apoptosome leads to their activation by dimerization. We investigated the influence of the coding CASP10 variant V410I (G1228A) by performing a case–control study — using 511 familial BC cases and 547 control subjects — on BC risk and revealed a significant association of V410I with a reduced risk (OR = 0.62, 95% CI = 0.43–0.88, P = 0.0076) related to the number of variant alleles (Ptrend = 0.0039). As CASP10 and CASP8 functionally co-operate during apoptosis, we analysed the mutual effect of both CASP10 V410I and CASP8 D302H, resulting in a significant association between the number of the variant alleles I410 and H302 and a highly decreased familial BC risk (OR = 0.35, Ptrend = 0.007), pointing to the interaction between the CASP10 and CASP8 polymorphisms in breast carcinogenesis.


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