AXIN2 Polymorphisms, the β-Catenin Destruction Complex Expression Profile and Breast Cancer Susceptibility
نویسندگان
چکیده
منابع مشابه
AXIN2 Polymorphisms, the β-Catenin Destruction Complex Expression Profile and Breast Cancer Susceptibility.
BACKGROUND The Wnt/β-catenin signaling pathway is an important regulator of cellular functions such as proliferation, survival and cell adhesion. Wnt/β-catenin signaling is associated with tumor initiation and progression; β-catenin mutations explain only 30% of aberrant signaling found in breast cancer, indicating that other components and/or regulation of the Wnt/β-catenin pathway may be invo...
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AIM OF THE STUDY To investigate the expression status and association of β-catenin and AXIN2 in ameloblastoma. MATERIAL AND METHODS 30 ameloblastoma specimens and 10 normal oral mucosa tissues were enrolled in the study. The protein and RNA levels of β-catenin and AXIN2 were detected by immunohistochemistry staining, Western blot, and real-time PCR analysis. The relationship between β-catenin...
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The objective of this study was to examine the expression and significance of β-catenin in the diagnosis and prognosis of breast cancer. Overall, 241 patients with histologically confirmed breast cancer who had undergone radical surgery were enrolled in this study. β-catenin protein expression in breast cancer samples was evaluated by immunohistochemistry. β-catenin was expressed in Nuclei/Plas...
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متن کاملAssociation of Genetic Variation in Genes Implicated in the B-Catenin Destruction Complex with Risk of Breast Cancer
Aberrant Wnt/B-catenin signaling leading to nuclear accumulation of the oncogene product B-catenin is observed in a wide spectrum of human malignancies. The destruction complex in the Wnt/B-catenin pathway is critical for regulating the level of B-catenin in the cytoplasm and in the nucleus. Here, we report a comprehensive study of the contribution of genetic variation in six genes encoding the...
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ژورنال
عنوان ژورنال: Asian Pacific Journal of Cancer Prevention
سال: 2015
ISSN: 1513-7368
DOI: 10.7314/apjcp.2015.16.16.7277