Abstract
The Wnt/beta-catenin signaling pathway is tightly regulated and has important functions in development, tissue homeostasis, and regeneration. Deregulation of Wnt/beta-catenin signaling is frequently found in various human cancers. Eighty percent of colorectal cancers alone reveal activation of this pathway by either inactivation of the tumor-suppressor gene adenomatous polyposis coli or mutation of the proto-oncogene beta-catenin. Activation of Wnt/beta-catenin signaling has been found to be important for both initiation and progression of cancers of different tissues. Therefore, targeted inhibition of Wnt/beta-catenin signaling is a rational and promising new approach for the therapy of cancers of various origins.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Adenomatous Polyposis Coli / drug therapy
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Adenomatous Polyposis Coli / metabolism*
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Antineoplastic Agents / pharmacology
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Antineoplastic Agents / therapeutic use
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Gene Expression Regulation, Neoplastic* / drug effects
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Gene Expression Regulation, Neoplastic* / genetics
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Humans
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Mutation
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Proto-Oncogene Mas
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Signal Transduction* / drug effects
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Signal Transduction* / genetics
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Tumor Suppressor Proteins / biosynthesis*
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Tumor Suppressor Proteins / genetics
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Wnt Proteins / antagonists & inhibitors
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Wnt Proteins / genetics
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Wnt Proteins / metabolism*
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beta Catenin / antagonists & inhibitors
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beta Catenin / genetics
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beta Catenin / metabolism*
Substances
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Antineoplastic Agents
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MAS1 protein, human
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Proto-Oncogene Mas
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Tumor Suppressor Proteins
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Wnt Proteins
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beta Catenin