Summary |
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Variant origin |
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Variant description |
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Tumor Data |
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Notes |
The gene that controls susceptibility to testosterone treatment is the gene that controls spontaneous tumor formation (J:9301). Three of the SWXJ recombinant inbred strains, along with the SWR/Bm progenitor, will produce granulosa cell (GC) tumors spontaneously, without DHEA treatment. Treatment with testosterone will also induce GC tumors, but only by increasing tumor incidence in those strains that are susceptible to spontaneous tumors (J:4202).
Mapping and Phenotype information for this QTL, its variants and associated markersJ:49710The authors analyzed three matings for genetic analysis to identify QTLs responsible for tumor susceptibility. 1) 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]. 2) The SWR congenic strains [SWR.SJL-X1, SWR.SJL-X2, SWR.SJL-X3, SWR.SJL-X4] containing most of Chromosome X from DXMit55 to DXMit182 and 3)SW x J RI strains. They were ableto identify a SJL derived susceptibility allele on mouse Chromosome X associated with DXMit16. The authors suggest that DXMit16 is not sufficient for tumorigenesis without the SWR susceptibility allele linked to D4Mit232. The authors also identified a parent of origin effect associated with the paternal allele of DXMit16 (chi square = 9.22; P<0.001). Thus females that inherited the SJL allele from the father have higher tumor incidences than those that inherit the allele from their mothers. An interesting candidate gene for Gct4 is the Ar locus which maps less than 1 cM proximal to DXMit16. |
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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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