Summary |
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Variant origin |
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Variant description |
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Phenotypes |
View phenotypes and curated references for all genotypes (concatenated display).
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Tumor Data |
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Notes |
Granulosa cell tumor susceptibility (Gct) controls granulosa cell carcinoma formation in response to dehydroepiandrosterone (DHEA) treatment. Spontaneous ovarian granulosa cell (GC) carcinomas occur in the inbred strain SWR/Bm and in three SWXJ recombinant inbred strains. Dehydroepiandrosterone (DHEA) treatment of the SWXJ recombinant inbred (RI) strains and of the progenitor strains SWR/Bm and SJL/Bm caused an increase in GC tumor incidence in SWR and in the RI strains that produced tumors spontaneously, and also caused tumors in five RI strains that had not previously produced GC tumors. The other SWXJ strains and the SJL/Bm progenitor strain did not produce tumors (J:9301).
Mapping and Phenotype information for this QTL, its variants and associated markersJ:49710The authors analyzed the F2 female progeny from four reciprocal F1 x F1 intercrosses [cross A. (SJL x SWR)F1 x (SJL x SWR)F1; cross B. (SJL x SWR)F1 x (SWR x SJL)F1; cross C. (SWR x SJL)F1 x (SJL x SWR)F1; cross D. (SWR x SJL)F1 x (SWR x SJL)F1] for granulosa cell (GC) tumors at 8 weeks of age to identify QTLs. D4Mit232 yielded the highest significance level of association GC tumorigenesis (chi square = 41.18; P<0.0001). The distal boundary of significant association with Gct has not been defined because of insufficient polymorphisms between SWR and SJL for loci distal to D4Mit190. The authors also found that at least one SWR-derived Gct allele is required for tumorigenesis and that this loci behaves like an oncogene with the SWR allele acting in a dominant fashion. |
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References |
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 11/12/2024 MGI 6.24 |
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