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Through studies using wild type and laboratory strains of mice, researchers have been able to model this disease.
We model this disease using the phase-field method and a set of diffusion reaction equations to account for the dynamics of nutrients and a key biomarker termed Prostate Specific Antigen.
Beyond transcriptional profiling and genomics datasets, there currently is no epigenome-scale dataset or integrative biology approach that can adequately model this disease and therefore identify novel mechanisms and targets for successful prevention and treatment of FL.
The mdx mouse, which is dystrophin-deficient, has long been used to model this disease.
While the therapeutics described above are currently in human clinical trials, it follows that there exists a need for efficient systems in which to model this disease.
Numerous approaches have been used to model this disease over the two decades since the identification of the t(8 21), with varying success and no accepted consensus as to which approach is both faithful to the human disease and relatively tractable as a model system (Hatlen et al, 2012).
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Modeling this disease in vitro using human cells is an important step toward identifying therapeutic interventions for HCM.
The deficits seen go beyond what one would expect from a mouse model of schizophrenia, thus questioning their utility as a selective model of this disease.
Three orthotopic CHS mouse models were published recently [ 8– 10] using CHS human cell lines, but there is no transgenic mouse model for this disease.
In this issue of Cancer Cell, Haldar et al. have genetically engineered a mouse model of this disease.
More than 50 years ago the owl monkey (genus Aotus) was found to be highly susceptible to developing human malaria, making it an excellent experimental model for this disease.
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