Daniel L Burgess


The availability of numerous existing inbred mouse strains and the practicality of maintaining large breeding colonies have made the mouse—because of its small size, rapid generation time, and low cost—an easy choice for biomedical researchers seeking animal models. These mouse strains exhibit wide differences in susceptibility to disorders that are important to humans: cancer, diabetes, obesity, cardiovascular and hematologic defects, developmental abnormalities, infertility, endocrine dysfunction, blindness, behavioral abnormalities, and epilepsy, among others. The cumulative health benefits that have been derived over the past century from studies using mice as models of human disease—to learn about pathologic mechanisms and develop new therapies—are incalculable, but they certainly surpass billions of health care dollars and millions of lives saved. Over the most recent decade, we witnessed what may be the most important advance yet for the study of mouse models of disease: the nearly simultaneous completion of the human and the mouse genome sequencing projects. Comparison of the two genomes indicates a remarkable degree of similarity; very few genes are present in one species that are not represented by orthologs in the other. Thus, one reason the mouse has provided such good models of human diseases is that the mouse genome is such a good model of the human genome!

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