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Model Characteristics - Model:
Nf1+/-KRas*
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| Model Descriptor |
Nf1+/-KRas*
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| Official Nomenclature |
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| Genotype |
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| Species |
Mouse (Mus musculus)
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| Strain |
Not specified
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| Is This a Tool Strain? |
No
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Developmental Stage
(applies only to Zebrafish) |
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| Experimental Design |
We analyzed three genetically engineered mouse (GEM) models of low-grade glioma resulting from either inactivation of the neurofibromatosis-1 (Nf1) tumor suppressor gene (a href=http://cancermodels.nci.nih.gov/camod/ViewModelAction.do?unprotected_method=populateModelCharacteristics&aModelID=50057313 target="_blank" Nf1+/-supGFAP/supCKO/a and a href=http://cancermodels.nci.nih.gov/camod/ViewModelAction.do?unprotected_method=populateModelCharacteristics&aModelID=50057345 target="_blank" Nf1+/-supGFAP-m/supCKO/a) or constitutive activation of KRas (Nf1+/-supKRas/sup) in glial cells. Based on tumor proliferation, location, and penetrance, we selected one GEM model, Nf1+/-supGFAP/supCKO, for preclinical drug evaluation.brbr
Nf1+/-supKRas*/sup mice were generated by successive breeding of Nf1+/- mice with LSL-KRassupG12D/sup mice and GFAP-Cre mice. Two other genetically engineered mouse models were also generated. This model was not chosen for preclinical trials to evaluate different therapeutic agents.
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| Phenotype |
Although the Nf1+/-KRas* model displayed many characteristics similar to human pediatric low-grade gliomas, this model was not chosen for preclinical evaluation. This model displays increased proliferation later in the time course than the chosen model.
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| Website for add. info |
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| Breeding Notes |
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| Sex Distribution of the Phenotype |
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| Submitted by |
caMOD, Curator
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| Principal Investigator / Lab |
Gutmann, David
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| Comment |
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| Model Availability: This model is available from |
| Strain |
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