Sistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSPFARIA, Paulo Rogerio deCHAMMAS, RogerMELO, Thaissa Lopes deHSU, Daniel K.LIU, Fu-TongNONOGAKI, SuelyCARDOSO, Sergio VitorinoLOYOLA, Adriano Mota2017-11-272017-11-272011EXPERIMENTAL AND MOLECULAR PATHOLOGY, v.90, n.2, p.189-193, 20110014-4800https://observatorio.fm.usp.br/handle/OPI/22897Background: Galectin-3 is a lectin that presents pivotal roles in tumor biology and there are no studies evaluating their expression in dysplasias and carcinomas developed from tongue carcinogenesis models. Aims: To investigate the role of galectin-3 in the development of tongue carcinomas using a mouse model of oral carcinogenesis. Methods: Galectin-3-deficient (gal3(-/-)) and wild-type (gal3(+/+)) mice were challenged with 4-nitroquinoline-1-oxide in drinking water for 16 weeks and killed at different times. Tongues were removed and the number of dysplasias and carcinomas was counted. An immunohistochemical study for galectin-3 was performed only in the tongue from gal3(+/+) mice. Results: In both groups, a reduction of dysplasias and an increase of carcinomas from week 16 to week 32 (p > 0.05) were observed. A predominance of high cytoplasmic and nuclear galectin-3 expression was observed in carcinomas (64.7%) and dysplasias (55.5%), respectively (p > 0.05). The perilesional areas always presented a statistical cytoplasmic and nuclear galectin-3 overexpression. Conclusions: Absence of galectin-3 did not directly affect the process of carcinogenesis and a cytoplasm shift of galectin-3 seems to be associated with development of tongue carcinomas.engrestrictedAccessOral carcinogenesisGalectin-3TongueMicePremalignant lesionsOral squamous cell carcinomasquamous-cell carcinomatargeted disruptionthyroid-carcinomatumor progressionexpressionnuclearheadlungdifferentiationlesionsarticleCopyright ACADEMIC PRESS INC ELSEVIER SCIENCE10.1016/j.yexmp.2010.12.007Pathology