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. 2009 Dec 1;69(23):9112-7.
doi: 10.1158/0008-5472.CAN-09-3342. Epub 2009 Nov 24.

Genetic factors on mouse chromosome 18 affecting susceptibility to testicular germ cell tumors and permissiveness to embryonic stem cell derivation

Philip D Anderson  1 , Vicki R Nelson, Paul J Tesar, Joseph H Nadeau
Affiliations

Genetic factors on mouse chromosome 18 affecting susceptibility to testicular germ cell tumors and permissiveness to embryonic stem cell derivation

Philip D Anderson et al. Cancer Res. .

Abstract

Despite strong heritability, little is known about the genetic control of susceptibility to testicular germ cell tumors (TGCT) in humans or mice. Although the mouse model of spontaneous TGCTs has been extensively studied, conventional linkage analysis has failed to locate the factors that control teratocarcinogenesis in the susceptible 129 family of inbred strains. As an alternative approach, we used both chromosome substitution strains (CSS) to identify individual chromosomes that harbor susceptibility genes and a panel of congenic strains derived from a selected CSS to determine the number and location of susceptibility variants on the substituted chromosome. We showed that 129-Chr 18(MOLF) males are resistant to spontaneous TGCTs and that at least four genetic variants control susceptibility in males with this substituted chromosome. In addition, early embryonic cells from this strain fail to establish embryonic stem cell lines as efficiently as those from the parental 129/Sv strain. For the first time, 129-derived genetic variants that control TGCT susceptibility and fundamental aspects of embryonic stem cell biology have been localized in a genetic context in which the genes can be identified and functionally characterized.

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Figures

Figure 1
Figure 1. TGCT data from adult parental strains and congenic strains
The sizes of the congenic intervals are shown relative to the two parent strains. M (MOLF/MOLF) and 1 (129/129) denote genotypes at each marker. The identities of the markers are listed in Supplemental Tables 3 and 4. The number of adult males surveyed and the number and percent of males affected with TGCTs is shown. The TGCT prevalences in the congenic strains were compared sequentially using the chi-square goodness-of-fit test or Fisher's Exact Test. P values have been corrected for eight tests and those with significant differences from control are listed. *not genotyped at this marker.
See this image and copyright information in PMC

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