ABSTRACT
Background: Oral cancer represents the sixth most common cancer in the world and is associated with 40-50%survival at 5 years. Within oral malignancies, oral squamous cell carcinoma (OSCC) is commonly preceded bypotentially malignant lesions, which, according to histopathological criteria, are referred to as oral dysplasia andtheir diagnosis are associated with higher rates of malignant transformation towards cancer. We recently reportedthat aberrant activation of the Wnt/β catenin pathway is due to overexpression of Wnt ligands in oral dysplasia.However, the expression of other regulators of this pathway, namely components of the β-catenin destructioncomplex has not been explored in oral dysplasia.Material and Methods: Using immunohistochemical analyses, we evaluated nuclear expression of β catenin andits association with Wnt3a and Wnt5a. Likewise, components of the β-catenin destruction complex, includingAdenomatous Polyposis Coli (APC), Axin and Glycogen Synthase Kinase 3 beta (GSK-3β) were also evaluatedin oral dysplasia and OSCC biopsies.Results: We found that moderate and severe dysplasia samples, which harbored increased expression of nuclearβ catenin, depicted augmented cytoplasmic expression of GSK 3β, Axin and APC, in comparison with OSCCsamples. Also, GSK-3β was found nuclear in mild dysplasia and OSCC samples, when compared with other studysamples.Conclusions: Cytoplasmic levels of components of the β-catenin destruction complex are increased in oral dyspla-sia and might be responsible of augmented nuclear β catenin.(AU)