Abstract
CDC25A is a critical regulator of cell cycle progression and checkpoint response. Overexpression of this cyclin-dependent kinase phosphatase occurs often in human cancers. Our recent genetic studies in the mouse indicate that restricting CDC25A can limit tumorigenesis induced by the HER2/neu-RAS oncogenic pathway without compromising normal cell division or viability. These findings offer a sound foundation to justify development of CDC25A inhibitors for antitumor therapy.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Review
MeSH terms
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Animals
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Cell Cycle
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Disease Progression
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Gene Expression Regulation, Enzymologic*
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Gene Expression Regulation, Neoplastic*
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Genome
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Genomic Instability
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Humans
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Mammary Neoplasms, Animal / genetics
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Mice
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Models, Biological
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Neoplasms / genetics*
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Neoplasms / metabolism*
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Receptor, ErbB-2 / metabolism
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cdc25 Phosphatases / chemistry
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cdc25 Phosphatases / physiology*
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ras Proteins / metabolism
Substances
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Receptor, ErbB-2
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cdc25 Phosphatases
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ras Proteins