Abstract
The Cre/loxP system is a powerful tool for generating conditional genomic recombination and is often used to examine the mechanistic role of specific genes in tumorigenesis. However, Cre toxicity due to its non-specific endonuclease activity has been a concern. Here, we report that tamoxifen-mediated Cre activation in vivo induced the regression of primary lymphomas in p53-/- mice. Our findings illustrate that Cre activation alone can induce the regression of established tumors.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antineoplastic Agents, Hormonal / pharmacology*
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Apoptosis / drug effects
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Carcinogenesis / genetics
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Enzyme Activation / drug effects
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Genetic Therapy
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Integrases / genetics*
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Integrases / metabolism
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Lymphoma / drug therapy*
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Lymphoma / genetics*
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Lymphoma / metabolism
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Lymphoma / pathology
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Magnetic Resonance Imaging
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Mice
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Mice, Knockout
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Promoter Regions, Genetic
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Tamoxifen / pharmacology*
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Tumor Burden / drug effects
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Tumor Suppressor Protein p53 / deficiency
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Tumor Suppressor Protein p53 / genetics*
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Ubiquitin C / genetics
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Ubiquitin C / metabolism
Substances
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Antineoplastic Agents, Hormonal
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Tumor Suppressor Protein p53
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Ubiquitin C
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Tamoxifen
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Cre recombinase
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Integrases