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UNC Lineberger

Genetically Engineered Mouse Models

Breast

 

  • C3(1)Tag – 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 – PMID 24220145). The C3(1)/Tag model is a non-hormone influenced model utilizing the 5’ 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 – PMID 10713685).  Importantly, inactivates of p53 and RB are known to be contribute to these important genetic lessons of human basal-like cancer.

 

  • MMTV-Neu – 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 neu transgene by mouse mammary tumor virus (MMTV) promoter.  (Guy et al., PNAS 1992 – PMID:  PMC50384).

 

  • MMTV-PyVT – A triple negative breast cancer model with a fast rate of metastasis.

Melanoma 

  • TRIA –  This model examines Tyr-Hras in mice with specific deficiencies of p16 Ink4A – and p19 Arf – (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). Nature, 413, 86–91.) 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.

 

 

  • Braf v600E; Pten; Tyr-Cre – 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 “leakiness” of the tyrosinase Cre. Homozygous Braf has a higher incidence of very aggressive tumor growth, therefore we maintain the line with heterozygous Braf.