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The laboratory mouse has been instrumental in investigating the genetics of human disease, including cancer, for over 110 years. [1] The laboratory mouse has physiology and genetic characteristics very similar to humans providing powerful models for investigation of the genetic characteristics of disease.
Patient derived xenografts (PDX) are models of cancer where the tissue or cells from a patient's tumor are implanted into an immunodeficient or humanized mouse. [1] It is a form of xenotransplantation. PDX models are used to create an environment that allows for the continued growth of cancer after its removal from a patient.
40% of both human and mouse genomes can be aligned at the nucleotide level. Mice have relatively short gestation periods. Mice take a brief time to reach sexual maturity. Mice have large litter sizes. The availability of hundreds of mutations affecting almost every tissue and aspect of development. Mice may not be an ideal model for breast cancer.
In spite of the efforts in developing this mouse model, poor engraftment of human hematopoietic stem cells (HSCs) was a major limitation that called for further advancement in the development humanized mouse models. [5] Nude mice were the earliest immunodeficient mouse model. These mice primarily produced IgM and had minimal or no IgA.
A genetically modified mouse, genetically engineered mouse model (GEMM) [1] or transgenic mouse is a mouse (Mus musculus) that has had its genome altered through the use of genetic engineering techniques. Genetically modified mice are commonly used for research or as animal models of human diseases and are also used for research on genes.
Human isogenic disease models have been likened to 'patients in a test-tube', since they incorporate the latest research into human genetic diseases and do so without the difficulties and limitations involved in using non-human models. [2] Historically, cells obtained from animals, typically mice, have been used to model cancer-related pathways.
For example, cancer therapies that exhibited promising results in mouse models can and have failed in clinical trials due to physiological differences in the activity of the targeted gene product. The activity of the mouse product did not translate to the activity of the human counterpart. [2]
In this model mutation in the Cdx2 gene in the Apc Δ716 mouse model shifted the formation of the polyps from the intestine to the colon, resembling the human FAP. The Apc mutant mice are characterized by early lethality. There are genes modifying the cancer susceptibility of these mouse models.
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