The following group of cancer mouse models may be used for identifying and/or screening of novel therapies in cancer, and tumor suppression:

• Hepsin overexpression: this transgenic model may be employed to investigate the function of hepsin in prostate cancer progression and serve as a system for testing novel antagonists or inhibitors.
• Delta-N-ERG: This prostate cancer model may be used to further delineate the roles that Delta-N-ERG plays in cancer progression and test the efficacy of anti-cancer therapies.
• Smo/Smo: Sonic Hedge Hog (Shh) and notch signaling is implicated in early hyperproliferation in medulloblastoma. This genetically faithful system may be employed for brain tumor therapy and/or drug screening for brain cancer prgression from early to late stages.
• P27S10A: This knock-in models may be used to examine the mechanisms underlying tumorgenesis for the development of novel therapies. This model provides a system with a S10A substutition mutation introduced into p27 is a useful tool for studying the mechanisms and signaling pathways involved in tumor resistance of various types of human cancers.
• P27CK-: The p27 CK- knock-in model has imparied p27, cyclin binding. This model may be used to examine the mechanisms underlying tumorgenesis for the development of novel therapies. These models provide a system to study the mechanisms and signaling pathways involved in tumor resistance of various types of human cancers.
• ErbB2: In addition to ErbB2 role in breast cancer and cardiomyopathy, these mice also provide a model for the study of treatments for the loss of motor and sensory neurons.
• VgEcR-RXR: A modified ecdysone receptor (VgEcR) and the retinoid X receptor (RXR) transgenic mouse serves as a system for examiing ecdysone-regulated gene expression in mammalian cells with implications for neuronal function, lipid metabolism, signaling, cell cycle regulation, embryonic development, cancer and apoptosis.
• GIST: This gastro-intestinal stromal tumor knock-in model with a mutation in the kit gene initially identified in sporadic gastrointestinal stromal tumors. This model may be used to examine the functional significance of Kit and for pre-clinical validation of novel gastrointestinal stromal tumor therapies.
• PMS-2: Mutations in the Pms2 DNA repair gene are responsible for many hereditary non-polyposis colorectal cancers. Mice deficient in Pms-2 may be used for drug screening of tumorcidal drugs, in particular for lymphoma and colorectal cancers. Model system for effect of diet in a cancer predisposing background.
• SK3 transgenic: The SK3 overexpression model may be used to investigate mechanisms that influence cardiomyopathy that may result from current cancer terapies. Sk3 is involved in the regulation of vaascular tone and blood pressue; thus modulation of its activity may help prevent cardiac dysfunction.

The mouse strains are fully developed and are available from The Jackson Laboratory.

Third Party Rights

The Howard Hughes Medical Institute and the United States Government provided funding for the development of these animal models.

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Please see downloads for associated academic references.

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