Sistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSPSOUZA, M. V. R.CHAMMAS, R.SANT'ANA, J. M. A.LOYOLA, A. M.CARDOSO, S. V.FARIA, P. R.2013-10-112013-10-112012HISTOPATHOLOGY, v.61, suppl.1, Special Issue, p.131-131, 20120309-0167https://observatorio.fm.usp.br/handle/OPI/2844Introduction: Oncogenic role for galectin-3 (GAL3) is due to its involvement in the Wnt signaling. Altered expression of Wnt-target proteins like cyclin D1 and APC promote malignant transformation. However, no study has hitherto showed whether GAL3 interferes in the expression of both proteins during oral carcinogenesis. This study reports cyclin D1 and APC expression in dysplasias and carcinomas induced in the tongue of galectin-3 deficient (GAL3)/)) and wild-type (GAL3+/+) mice. Material and Methods: Sixty GAL3)/) and GAL3 +/+ mice were treated with 4NQO for 16 weeks and killed at week 16 and week 32. The tongues were removed and processed for paraffin embedding. Sections were stained with Haematoxylin and Eosin to identify dysplasias and carcinomas. An immunohistochemical assay was applied to evaluate the expression of cyclin D1 and APC protein. Results: Oral carcinogenesis occurred in both groups (P> 0.05). In GAL3)/) mice, the percentage of cyclin D1-positive cells was 36% for both dysplasias and carcinomas; in GAL3 +/+ mice, it was 28% and 34%, respectively. The intensity of APC expression in dysplasias from GAL3)/) mice ranged from weak (31.7%), moderate (12.2%) to strong (2.4%); in carcinomas from the same group, 48.1% and 7.4% of cases respectively exhibited a weak and moderate expression. In GAL3 +/+ mice, 59.4% and 28.1% of dysplasias and 50% and 40% of carcinomas presented a weak and moderate APC expression, respectively. However, no statistical significance was found. Conclusion: The absence of GAL3 does not interfere in the oral carcinogenesis and activated Wnt signaling was observed in both groups of mice (FAPEMIG).engrestrictedAccessconferenceObjectCopyright WILEY-BLACKWELLCell BiologyPathology