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Mapping Data
Experiment
  • Experiment
    TEXT-QTL
  • Chromosome
    11
  • Reference
    J:193231 Okumura K, et al., Independent genetic control of early and late stages of chemically induced skin tumors in a cross of a Japanese wild-derived inbred mouse strain, MSM/Ms. Carcinogenesis. 2012 Nov;33(11):2260-8
  • ID
    MGI:5795898
Genes
GeneAlleleAssay TypeDescription
Stmm5 visible phenotype
Notes
  • Experiment
    To identify genetic determinants of skin cancer susceptibility and carcinoma development, a large backcross population of FVB/NJcl x (FVB/NJcl x MSM/Ms) F1 mice were subjected to DMBA/TPA-induced skin carcinogenesis. MSM/Ms mice are more resistant to chemically induced skin tumor development than the highly susceptible FVB/N strain.

    (FVB/NJcl x MSM/Ms) male mice were backcrossed with female FVB/NJcl mice generating 121 F1 Tpr53 homozygous mice, p53+/+. Tpr53 deficient male mice (FVB/NJcl x MSM.Cg-Trp53tm1Sia/+) were backcrossed to female FVB/NJcl mice generating 107 Tpr53 heterozygous F1 backcross mice, p53+/-. Mice were genotyped using PCR assays.

    Tumor development was monitored for a period of 40 weeks; the number of papillomas at 20 weeks as well as the presence of carcinomas at 40 weeks was documented. In addition papillomas were categorized into three groups based on diameter size, <2mm, 2-6mm and >6mm. All mice were genotyped using 107 SNP markers distributed evenly over the genome.

    QTL Stmm5, skin tumor modifier of MSM 5 was identified in the FVB/NJcl x (FVB/NJcl x MSM.Cg-Trptm1Sia/+)F1 backcrossed mice. Stmm5 was a measure of the total number of papillomas at 20 weeks, LOD=3.55 mapping with peak marker D11SNP8 (rs3023316) at 86.4 cM on Chromosome 11. Approximately 93 percent of mice without tumors at this locus were heterozygous with FVB/MSM alleles. [Table 1.]


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last database update
11/12/2024
MGI 6.24
The Jackson Laboratory