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Human Molecular Genetics, 2003, Vol. 12, No. 4 389-398
© 2003 Oxford University Press

Testicular cancer susceptibility in the 129.MOLF-Chr19 mouse strain: additive effects, gene interactions and epigenetic modifications

Kirsten K. Youngren1, Joseph H. Nadeau1,* and Angabin Matin2,*

1Department of Genetics, Case Western Reserve University School of Medicine and Center for Human Genetics and Ireland Cancer Center, University Hospitals of Cleveland, Cleveland, Ohio, USA and 2Department of Molecular Genetics, Section of Cancer Genetics, University of Texas, MD Anderson Cancer Center, Houston, Texas, USA

Received September 4, 2002; Accepted December 16, 2002

Testicular germ cell tumors (TGCTs) are the most common solid cancers affecting young men. Although the evidence for genetic predisposition to TGCTs in humans is compelling, the genetic control of susceptibility is poorly understood. The 129S1/SvImJ (129/Sv) inbred strain of mice is an excellent model for studying TGCT susceptibility. We previously reported a new mouse strain, the 129.MOLF-Chr19 chromosome substitution strain, which develops spontaneous TGCTs at a high frequency (70–80%) as compared with the much lower rate in the 129/Sv strain (5%). To characterize the genetic control of TGCT susceptibility, we created a panel of single- and double-congenic strains derived from 129.MOLF-Chr19. The frequency of TGCTs in these strains suggests that several genes with additive and epistatic effects located at distinct sites on chromosome 19 control susceptibility. However, an alternative interpretation involving epigenesis is based on a striking correlation between TGCT frequency and the length of the MOLF-derived congenic segment, regardless of their chromosomal location on Chr 19 in each congenic strain. We also show that bilateral TGCT cases result from the coincidental co-occurrence of unilateral TGCTs rather than from the action of distinct genes that control susceptibility to bilateral versus unilateral TGCT cases. Finally, we propose that these TGCTs result from disrupted testicular and spermatogenic developmental programs.

* To whom correspondence should be addressed at: Department of Genetics, CWRU School of Medicine, 10900 Euclid Ave, Cleveland, OH 44106, USA. Tel: +1 2163680581; Fax: +1 2163683432; Email: jhn4{at}po.cwru.edu; and Dept. of Molecular Genetics, Section of Cancer Genetics. Tel: +1 7137945250; Email: amatin{at}mail-mdanderson.org


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