Abstract
Two non-inbred mouse lines, phenotypically selected for maximal (AIRmin) and minimal (AIRmax) acute inflammatory response, show differential susceptibility/resistance to the development of several chemically-induced tumor types. An intercross pedigree of these mice was generated and treated with the chemical carcinogen dimethylhydrazine, which induces lung and intestinal tumors. Genome wide high-density genotyping with the Restriction Site-Associated DNA genotyping (2B-RAD) technique was used to map genetic loci modulating individual genetic susceptibility to both lung and intestinal cancer. Our results evidence new common quantitative trait loci (QTL) for those phenotypes and provide an improved understanding of the relationship between genomic variation and individual genetic predisposition to tumorigenesis in different organs.
Highlights
This study aimed to map chromosomal regions involved in the regulation of susceptibility/resistance of mice in developing colon and lung tumors, induced by treatment with chemical carcinogen
Colon and lung carcinogenesis The phenotypic characterization was performed in the pedigree consisting of AIRmax, AIRmin grandparents (n = 22), (AIRmax x AIRmin)F1 parents (n = 20), and (AIRmax x AIRmin)F2 (n = 180) animals to evaluate the association between the transmitted alleles and the phenotypes presented by the individuals
The AIRmax and AIRmin mouse lines are powerful for this type of research since they differ widely in resistance/susceptibility to development of lung and colon tumors
Summary
This study aimed to map chromosomal regions involved in the regulation of susceptibility/resistance of mice in developing colon and lung tumors, induced by treatment with chemical carcinogen. Previous mapping studies using several inbred susceptible and resistant mouse lines and crosses, as well as recombinant congenic strains (CcS/Dem), identified about 20 regions distributed across the chromosomes containing candidate modifier genes of colon carcinogenesis. The susceptibility of AIRmax and AIRmin mice to develop tumors in the colon and lungs after treatment with the same carcinogen (DMH) makes the model suitable for the research of common genes involved in their regulation. For this we produced, an (AIRmax x AIRmin) F2 population and treated all F2 animals with (DMH). Highdensity genotyping was carried out for all individuals with the 2BRAD technique (Restriction Site-Associated DNA genotyping) [13,14,15], to map the genetic loci that modulate individual susceptibility to colon and lung cancer
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