β-Catenin pathway activation in breast cancer is associated with triple-negative phenotype but not with CTNNB1 mutation

Aberrant β -catenin expression as determined by assessment of its subcellular localization constitutes a surrogate marker of Wnt signalling pathway activation and has been reported in a subset of breast cancers. The association of β -catenin/Wnt pathway activation with clinical outcome and the mecha...

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Published in:Modern pathology 2011-02, Vol.24 (2), p.209-231
Main Authors: Geyer, Felipe C, Lacroix-Triki, Magali, Savage, Kay, Arnedos, Monica, Lambros, Maryou B, MacKay, Alan, Natrajan, Rachael, Reis-Filho, Jorge S
Format: Article
Language:English
Subjects:
631/208/737
631/80/86
692/699/67/1347
beta Catenin - genetics
beta Catenin - metabolism
Biomarkers, Tumor - genetics
Biomarkers, Tumor - metabolism
Breast Neoplasms - genetics
Breast Neoplasms - metabolism
Carcinoma - genetics
Carcinoma - metabolism
DNA Mutational Analysis
Female
Humans
Immunohistochemistry
Laboratory Medicine
Medicine
Medicine & Public Health
Mutation
original-article
Pathology
Phenotype
Signal Transduction - physiology
Survival Analysis
Tissue Array Analysis
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Summary:Aberrant β -catenin expression as determined by assessment of its subcellular localization constitutes a surrogate marker of Wnt signalling pathway activation and has been reported in a subset of breast cancers. The association of β -catenin/Wnt pathway activation with clinical outcome and the mechanisms leading to its activation in breast cancers still remain a matter of controversy. The aims of this study were to address the distribution of β -catenin expression in invasive breast cancers, the correlations between β -catenin expression and clinicopathological features and survival of breast cancer patients, and to determine whether aberrant β -catenin expression is driven by CTNNB1 ( β -catenin encoding gene) activating mutations. Immunohistochemistry was performed on a tissue microarray containing 245 invasive breast carcinomas from uniformly treated patients, using two anti- β -catenin monoclonal antibodies. Selected samples were subjected to CTNNB1 exon 3 mutation analysis by direct gene sequencing. A good correlation between the two β -catenin antibodies was observed (Spearman's r >0.62, P
ISSN:0893-3952
1530-0285
DOI:10.1038/modpathol.2010.205