The EMSS laboratory offers established GEM models to investigate prevention, intervention and regression studies. The EMSS offers in vivo cancer models in Breast and Colon cancer plus other GEM models which can be implanted with the wide variety of human cancer cell lines. The EMSS is able to complete experiments in any established GEM model and to create new GEM models using established lines.
Last updated 9/30/09.
Cancer Type |
Model Name |
Genetic Model Type |
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MMTV-pyMT |
Transgenic |
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Mouse mammary tumor virus (MMTV) LTR enhancer drives expression to the mammary gland in this model. The Polyoma middle T antigen (pyMT) is a highly oncogenic protein that directly activates the AKT and src pathways, among others (ref). This model, established in 1992 in the Muller lab (ref), is highly representative of human breast cancer (ref), and spontaneously generates mammary gland tumors that metastasize to the lung. Tumors arise with a median onset of 8-12 weeks in virgin females. It is a useful GEM model to understand the mechanisms of the process of metastasis from primary tumor in breast cancer progression. |
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COLON |
C57BL6/J-ApcMin/+ |
Induced mutation |
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This is a model for human Familial Adenomatous Poliposis (FAP). Patients with FAP have a germ-line inactivation of one allele in the Adenomatuous Polyposis Coli (APC) tumor suppressor gene and develop multiple colonic adenomatous polyps early in life with progression to malignant tumors. ApcMin/+ or Min (multiple intestinal neoplasia) mice have a nonsense mutation in codon 850 of the mouse Apc gene (Moser et al, Science, 1990, 322-324). The mutation was chemically induced, although not targeted. Mice develop multiple benign tumors mostly in the small intestine (on average 40 per mouse) and a few colonic tumors (1-3 per mouse) and usually die by 120 days of age from bowel obstruction. ApcMin/+ mice may develop anemia and females mice may spontaneously develop mammary tumors. These mice are maintained on the C57/BL6/J background by breeding heterozygote males to wild type females (homozygote ApcMin/+ mice are not viable). |
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B6.129 Kras |
Knock in |
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These mice carry a latent point-mutant allele of oncogenic K-ras2 (K-rasG12D). Cre-mediated recombination leads to deletion of a transcriptional termination sequence (Lox-Stop-Lox) and expression of the oncogenic protein. By crossing to a tissue-specific cre, you can generate any tissue lung specific model, including lung models (Promoter) and pancreas model (P48-cre). The lung model was established in the Jacks lab (ref.) in 2001, and the pancreas model was published in the Tuveson lab (ref.) in 2003. It is a useful GEM model that allows one to characterize stages of ras-dependent tumor progression. |
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PANCREATIC |
pdx-cre |
Transgenic |
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Cre recombinase induces the release of genes that are floxed. Pdx-1-Cre mice exhibit a stochastic pattern of high-level Cre expression in the pancreas (Hingorani et al., 2003). When combined with Tyler Jacks' latent activatable K-ras allele, LSL-KrasG12D (Kras2, MMHCC strain code 01XJ6), Pdx-1-Cre causes ductal lesions that recapitulate the full spectrum of human pancreatic intraepithelial neoplasias (PanINs). Some of these lesions progress to invasive and metastatic adenocarcinomas. These mice are currently on a B6.FVB background and are being backcrossed further onto the B6 background. |
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