C3(1)Tag\u00a0<\/strong>\u2013\u00a0<\/strong>This model is similar to the human Triple negative breast cancer of basal-like sub-type as shown by gene expression analysis (Pfefferele et al., Genome Biology 2013<\/em>\u00a0\u2013 PMID 24220145). The C3(1)\/Tag model is a non-hormone influenced model utilizing the 5\u2019 flanking region of the C3(1) component of the rat prostate steroid binding protein (PSBP) to target the expression of Simian Virus 40 (SV40) large T-antigen (Tag) to the epithelium of both the mammary and prostate glands. SV40 large Tag has been shown to inactivate both p53 and RB (Green et al., Oncogene 2000<\/em>\u00a0\u2013 PMID 10713685). \u00a0Importantly, inactivates of p53 and RB are known to be contribute to these important genetic lessons of human basal-like cancer.<\/li>\n<\/ul>\n
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MMTV-Neu \u2013\u00a0<\/strong>The Neu model represents HER2 positive breast cancer tumors. It is an autochthonous breast cancer model that is driven by over-expression a non-activated Rat\u00a0neu<\/em>\u00a0transgene by mouse mammary tumor virus (MMTV) promoter.\u00a0 (Guy et al., PNAS 1992 \u2013 PMID:\u00a0 PMC50384).<\/li>\n<\/ul>\n
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MMTV-PyVT \u2013\u00a0<\/strong>A triple negative breast cancer model with a fast rate of metastasis.<\/li>\n<\/ul>\n
Melanoma\u00a0<\/h2>\n
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TRIA \u2013 \u00a0<\/strong>This model examines Tyr-Hras in mice with specific deficiencies of p16 Ink4A \u2013 and p19 Arf \u2013 (Loss of p16Ink4a With Retention of p19Arf Predisposes Mice to Tumorigenesis Sharpless NE, Bardeesy N, Lee KH, Carrasco D, Castrillon DH, Aguirre AJ, Wu EA, Horner JW and DePinho RA . (2001).\u00a0Nature<\/i>,\u00a0413<\/b>, 86\u201391.) All male animals carry the Hras mutation and both Ink and Arf have been knocked out. Latency with the TRIA is 14-20 weeks with approximately 80% penetrance and the tumors generally present on the pinnia and tail.<\/li>\n<\/ul>\n
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Braf v600E; Pten; Tyr-Cre \u2013\u00a0<\/strong>This inducible Cre recombinant model deletes Pten to drive expression of Braf in site specific tumorigenesis. Using topically applied tamoxifen at the base of the tail, a pigmented tumor will present in 4-8 weeks. The ptenbraf model is susceptible to spontaneous secondary tumors due to the potential \u201cleakiness\u201d of the tyrosinase Cre. Homozygous Braf has a higher incidence of very aggressive tumor growth, therefore we maintain the line with heterozygous Braf.<\/li>\n<\/ul>\n","protected":false},"excerpt":{"rendered":"