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Carcinogenesis Advance Access published online on June 23, 2005
Carcinogenesis, doi:10.1093/carcin/bgi164
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oupjournals.org
Received April 25, 2005
Revised June 6, 2005
Accepted June 15, 2005

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

Association of death receptor 4 haplotype 626C-683C with an increased breast cancer risk

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

1 Division of Molecular Genetic Epidemiology, German Cancer Research Center, Heidelberg, Germany
2 Division of Molecular Genetic Epidemiology, German Cancer Research Center, Heidelberg, Germany; Department of Biosciences at Novum, Karolinska Institute, Huddinge, Sweden
3 Department of Gynaecology and Obstetrics, Klinikum rechts der Isar at the Technical University, Munich, Germany
4 Institute of Human Genetics, University of Heidelberg, Heidelberg, Germany
5 Division of Molecular Gynaeco-Oncology, Department of Gynaecology and Obstetrics, Clinical Center University of Cologne, Germany
6 Department of Gynaecology and Obstetrics at the Ludwig-Maximilians-University, Munich, 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

* To whom correspondence should be addressed.
Bernd Frank, E-mail: b.frank{at}dkfz.de


  Abstract

Dysregulation of apoptosis plays a crucial role in carcinogenesis. Tumour necrosis factor-related apoptosis-inducing ligand TRAIL stimulates the extrinsic apoptotic pathway by binding to death receptor 4 (DR4). Thus, genetic alterations within the candidate tumour suppressor gene DR4 would be expected to provoke a deficient apoptotic signalling thereby facilitating the development of cancer. The DR4 variants Thr209Arg and Glu228Ala were genotyped in a series of 521 breast cancer cases and 1100 control subjects from Germany determining their impact on breast cancer risk. Neither Thr209Arg (626C>G) nor Glu228Ala (683A>C) alone were significantly associated with breast cancer risk (OR = 0.84, 95% CI = 0.65-1.08, P = 0.18 and OR = 0.89, 95% CI = 0.72-1.12, P = 0.30). Haplotype analysis, however, revealed a 3.5-fold risk for carriers of the 626C-683C haplotype (OR = 3.52, 95% CI = 1.45-8.52, P = 0.003).


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[Abstract] [Full Text] [PDF]


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