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Annals of Oncology Advance Access originally published online on July 15, 2008
Annals of Oncology 2008 19(11):1910-1914; doi:10.1093/annonc/mdn407
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© The Author 2008. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org

urogenital tumors

Association of the polymorphism of the CAG repeat in the mitochondrial DNA polymerase gamma gene (POLG) with testicular germ-cell cancer

M. Blomberg Jensen1,*, H. Leffers1, J. H. Petersen1,2, G. Daugaard3, N. E. Skakkebaek1 and E. Rajpert-De Meyts1,*

1 University Departments of Growth & Reproduction
2 Biostatistics
3 Oncology, Rigshospitalet and Copenhagen University, Copenhagen, Denmark

* Correspondence to: Dr M. B. Jensen, Department of Growth and Reproduction, Rigshospitalet, Blegdamsvej, Copenhagen 2200, Denmark. Tel: 35455017; Fax: 35456054; E-mail: blombergjensen{at}gmail.com

Background: A possible association between the polymorphic CAG repeat in the DNA polymerase gamma (POLG) gene and the risk of testicular germ-cell tumours (TGCT) was investigated in this study. The hypothesis was prompted by an earlier preliminary study proposing an association of the absence of the common 10-CAG-long POLG allele with testicular cancer as well as previously reported in some European populations’ association with male subfertility, which is a condition carrying an increased risk of TGCT.

Patients and methods: The number of CAG repeats in both POLG alleles was established in 243 patients with TGCT and in 869 controls by the analysis of the genomic DNA fragment.

Results: A significantly higher proportion of men homozygous allele of other than the common 10 CAG repeats was found among the patients with TGCT in comparison to the controls (4.9% versus 1.3%, respectively, P = 0.001). The vast majority of the homozygous patients had a seminoma (11 of 12; 97%), despite that only about half (55%) of the studied patients had this tumour type.

Conclusions: The findings indicate that the POLG polymorphism may be a contributing factor in the pathogenesis of TGCT particularly in seminoma, but the mechanisms remain to be elucidated.

Key words: CAG repeat, mitochondria, POLG gene, seminoma, testicular dysgenesis syndrome, testicular neoplasm

Received for publication February 20, 2008. Revision received April 25, 2008. Accepted for publication June 4, 2008.


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