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Human Molecular Genetics Advance Access originally published online on July 6, 2005
Human Molecular Genetics 2005 14(16):2349-2356; doi:10.1093/hmg/ddi237
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© The Author 2005. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

Allelic association of the human homologue of the mouse modifier Ptprj with breast cancer

Fabienne Lesueur1,*, Paul D. Pharoah1, Stewart Laing1, Shahana Ahmed1, Clare Jordan1, Paula L. Smith2, Robert Luben3, Nicholas J. Wareham3, Douglas F. Easton2, Alison M. Dunning1 and Bruce A.J. Ponder1

1 Cancer Research UK Human Cancer Genetics Research Group, Department of Oncology, University of Cambridge, Cambridge CB2 1TN, UK, 2 Cancer Research UK Genetic Epidemiology Group, Department of Public Health and Primary Care, University of Cambridge, Cambridge CB2 1TN, UK and 3 MRC Epidemiology Unit, Strangeways Research Laboratories, Cambridge CB1 8RN, UK

* To whom correspondence should be addressed at: CNRG, Centre National de Génotypage, 91057 Evry Cedex, France. Tel: +33 160878433; Fax: +33 160878383; Email: fabienne.lesueur{at}cng.fr

Received May 18, 2005; Revised June 21, 2005; Accepted June 29, 2005

Human homologues of mouse cancer modifier genes may play a role in cancer risk and prognosis. A proportion of the familial risk of common cancers may be attributable to variants in such genes, each contributing to a small effect. The protein tyrosine phosphatase receptor type J (PTPRJ) has been recently identified as being the protein encoded by the Scc1 mouse gene (susceptibility to colon cancer-1). In addition, the PTPRJ gene has been shown to be somatically altered in several human cancer types such as colon, lung and breast cancers and to have the characteristics of a tumour-suppressor gene. The purpose of this study was to determine whether common variants in the PTPRJ gene represent low penetrance breast cancer susceptibility alleles. To test this hypothesis, we assessed single nucleotide polymorphisms (SNPs) tagging the common SNPs and haplotypes of the gene in 4512 cases and 4554 controls from the East Anglian population. We observed a difference in the haplotype frequency distributions between cases and controls (P=0.0023, OR=0.81 [0.72–0.92]). Thus, carrying a specific PTPRJ haplotype confers a protective effect on the risk of breast cancer. This result establishes the principle that mouse cancer modifier genes are candidates for low penetrance human breast cancer susceptibility genes.


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