Mapping Data

Experiment

• Experiment
  TEXT-QTL-Candidate Genes
• Chromosome
  16
• Reference
  J:85134 Nagase H, et al., Allele-specific Hras mutations and genetic alterations at tumor susceptibility loci in skin carcinomas from interspecific hybrid mice. Cancer Res. 2003 Aug 15;63(16):4849-53
• ID
  MGI:3055782

Genes

Gene	Assay Type
D16Mit2	PCR amplified length variant
Skts9	resistance/susceptibility

Notes

• Experiment
  Several skin tumor susceptibility QTLs (Skts1-Skts13) were previously identified in a population of (NIH/Ola x M. spretus)F1 x NIH/Ola backcross animals. In this study the association of allele-specific mutations at the Skts intervals was examined in skin carcinoma samples. Several loci displayed allelic loss or duplication in skin carcinomas.
  
  90 % of papillomas and carcinomas contain a mutation at codon 61 of the Hras1 gene (72 cM). In 23 out of 26 mouse tumors the Hras1 mutation occurred in the NIH/Ola-inherited allele. Hras1 maps near skin tumor susceptibility QTL Skts2 (64 cM on mouse Chromosome 7). A nearby marker, D7Mit12 (66 cM) also shows allelic imbalance involving the NIH/Ola allele.
  
  On mouse Chromosome 6, preferential gain of the M. spretus allele or loss of the NIH/Ola allele was observed at D6Mit9 (36.5 cM) near Skts11 in 21 out of 21 carcinomas, and preferential gain of the M. spretus allele was observed at D6Mit15 (74 cM) near Skts12 in 14 out of 16 carcinomas.
  
  On mouse Chromosome 9, preferential loss of the M. spretus allele or gain of the NIH/Ola allele was observed at D9Mit9 (48 cM) near Skts6 in 16 out of 23 carcinomas.
  
  On mouse Chromosome 16, preferential loss of the M. spretus allele or gain of the NIH/Ola allele was observed at D16Mit2 (14.1 cM) near Skts9 in 10 out of 29 carcinomas.