Abstract
Increased transcriptional activation through beta-catenin stabilization plays a central role in colorectal tumorigenesis. Alterations of phosphorylation sites within the CTNNB1 gene, which codes for beta-catenin has been reported to occur in about one-half of colorectal tumors without APC-gene mutations. We assessed the importance of mutations in the regulatory domain, located within exon 3 of CTNNB1, in 103 rectal carcinomas and correlated these data with presence of microsatellite instability, somatic frame-shift alterations of the TCF-4 gene, and APC-gene mutations in the tumors. No mutation was detected in exon 3 of the CTNNB1 gene and our results thus demonstrate that beta-catenin activation through mutation rarely contributes to the development of sporadic and microsatellite instability stable rectal cancer.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenocarcinoma / genetics*
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Adenocarcinoma / metabolism
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Adult
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Aged
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Aged, 80 and over
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Chromosome Aberrations / genetics*
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Cytoskeletal Proteins / genetics*
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Cytoskeletal Proteins / metabolism
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DNA Primers / chemistry
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Female
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Frameshift Mutation / genetics
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Genes, APC / genetics
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Humans
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Male
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Microsatellite Repeats / genetics
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Middle Aged
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Mutation*
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Polymerase Chain Reaction
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Rectal Neoplasms / genetics*
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Rectal Neoplasms / metabolism
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TCF Transcription Factors
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Trans-Activators*
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Transcription Factor 7-Like 2 Protein
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Transcription Factors / genetics
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beta Catenin
Substances
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CTNNB1 protein, human
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Cytoskeletal Proteins
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DNA Primers
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TCF Transcription Factors
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TCF7L2 protein, human
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Trans-Activators
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Transcription Factor 7-Like 2 Protein
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Transcription Factors
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beta Catenin