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Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06520 [G. G-R., G. T., T. G. D., M. L. C., D. L. R.], and Department of Pathology, Oviedo University School of Medicine, 33006, Asturias, Spain [A. H.]
ß-catenin is an ubiquitously expressed cytoplasmic protein that has a crucial role in both E-cadherin-mediated cell-cell adhesion and as a downstream signaling molecule in the wingless pathway. Stabilization of ß-catenin followed by nuclear translocation and subsequent T-cell factor/lymphoid-enhancing factor-mediated transcriptional activation has been proposed as an important step in oncogenesis. Stabilization may occur through activating mutations in exon-3 at the phosphorylation sites for ubiquitination and degradation of ß-catenin. Immunohistochemical subcellular localization of ß-catenin and mutational analysis of exon-3 of the ß-catenin gene by single-strand conformational polymorphism followed by DNA sequencing was performed on 37 samples from 31 patients with anaplastic thyroid carcinoma. Immunofluorescent staining showed nuclear localization in 15 (42%) of the 36 samples examined. Nucleotide sequencing of mobility shifts detected by single-strand conformational polymorphism revealed somatic alterations in 19 (61%) of the 31 patients analyzed. We conclude that mutations in ß-catenin are common in anaplastic thyroid cancer and that they may activate transcription, as illustrated by frequent nuclear localization of the protein. These findings support the idea that ß-catenin acts as an oncogene and contributes to the highly aggressive behavior of this tumor.
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J. Böhm, L. Niskanen, K. Kiraly, J. Kellokoski, M. Eskelinen, S. Hollmen, E. Alhava, and V.-M. Kosma Expression and Prognostic Value of {{alpha}}-, {beta}-, and {{gamma}}-Catenins in Differentiated Thyroid Carcinoma J. Clin. Endocrinol. Metab., December 1, 2000; 85(12): 4806 - 4811. [Abstract] [Full Text]
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P. W. Schlosshauer, S. A. Brown, K. Eisinger, Q. Yan, E. R. Guglielminetti, R. Parsons, L. H. Ellenson, and J. Kitajewski APC truncation and increased {beta}-catenin levels in a human breast cancer cell line Carcinogenesis, July 1, 2000; 21(7): 1453 - 1456. [Abstract] [Full Text] [PDF]
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F. T. Kolligs, B. Kolligs, K. M. Hajra, G. Hu, M. Tani, K. R. Cho, and E. R. Fearon gamma -Catenin is regulated by the APC tumor suppressor and its oncogenic activity is distinct from that of beta -catenin Genes & Dev., June 1, 2000; 14(11): 1319 - 1331. [Abstract] [Full Text]
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O. Gimm, A. Perren, L.-P. Weng, D. J. Marsh, J. J. Yeh, U. Ziebold, E. Gil, R. Hinze, L. Delbridge, J. A. Lees, et al. Differential Nuclear and Cytoplasmic Expression of PTEN in Normal Thyroid Tissue, and Benign and Malignant Epithelial Thyroid Tumors Am. J. Pathol., May 1, 2000; 156(5): 1693 - 1700. [Abstract] [Full Text] [PDF]
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H. Huang, H. Fujii, A. Sankila, B. M. Mahler-Araujo, M. Matsuda, G. Cathomas, and H. Ohgaki {beta}-Catenin Mutations Are Frequent in Human Hepatocellular Carcinomas Associated with Hepatitis C Virus Infection Am. J. Pathol., December 1, 1999; 155(6): 1795 - 1801. [Abstract] [Full Text] [PDF]
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