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Manipulation of the mouse germline in the study of Min-induced neoplasia
A Bilger1, A R Shoemaker, K A Gould
1Laboratory of Genetics, University of Wisconsin Medical School, Madison 53706, USA.
Abstract:
The Min mouse, generated by random germline mutagenesis, carries a mutation in the mouse homolog of APC and is a model of inherited human intestinal tumorigenesis. To identify other genes in the pathway(s) of intestinal tumorigenesis, genes that modify the Min phenotype have been sought. Several have been identified, including Mom1 and the genes for the 5-cytosine DNA methyltransferase and the DNA mismatch repair factor Msh2. Min-dependent tumorigenesis also occurs in mammary glands, the pancreas, and the body wall. The Min mouse has therefore become a model for tumorigenesis in a variety of organs. Identifying modifiers of its phenotype will help in piecing together the pathways of tumorigenesis in each of these tissues.
Insights
The Min mouse, a model for human intestinal cancer, helps identify genes involved in tumor development. Studying these modifier genes reveals pathways crucial for understanding tumorigenesis across multiple organs.
Area of Science:
- Genetics
- Cancer Biology
- Mouse Models
Background:
- The Min mouse carries a mutation in the Apc gene, serving as a model for inherited human intestinal cancer.
- Tumorigenesis in Min mice is not limited to the intestine, also occurring in mammary glands, pancreas, and body wall.
Purpose of the Study:
- To identify genes that modify the Min phenotype, thereby uncovering pathways involved in intestinal tumorigenesis.
- To expand the understanding of tumorigenesis across various organs using the Min mouse model.
Main Methods:
- Germline mutagenesis was employed to generate the Min mouse model.
- Phenotypic analysis of Min mice was conducted to identify genetic modifiers.
Main Results:
- Several modifier genes, including Mom1, 5-cytosine DNA methyltransferase, and Msh2, have been identified.
- Min-dependent tumorigenesis was observed in multiple organs beyond the intestine.
Conclusions:
- The Min mouse is a valuable model for studying inherited intestinal cancer and tumorigenesis in other tissues.
- Identifying phenotype modifiers is crucial for elucidating the complex pathways of tumorigenesis in different organs.