Abstract
BackgroundDeregulation of ?-catenin is associated with malignant transformation; however, its relationship with potentially malignant and malignant oral processes is not fully understood. The aim of this study was to determine and compare the nuclear ?-catenin expression in oral dysplasia and oral squamous cell carcinoma (OSCC). Material and MethodsCross sectional study. Immunodetection of ?-catenin was performed on 72 samples, with the following distribution: 21 mild dysplasia, 12 moderate dysplasia, severe dysplasia 3, 36 OSCC including 19 well differentiated, 15 moderately differentiated and 2 poorly differentiated. Through microscopic observation the number of positive cells per 1000 epithelial cells was counted. For the statistical analysis, the Kruskal Wallis test was used.ResultsNuclear expression of ?-catenin was observed in all samples with severe and moderate dysplasia, with a median of 267.5, in comparison to mild dysplasia whose median was 103.75. Only 10 samples (27.7%) with OSCC showed nuclear expression, with statistically significant differences between groups (p < 0.05).ConclusionsOur results are consistent with most of the reports which show increased presence of ?-catenin in severe and moderate dysplasia compared to mild dysplasia; however the expression of nuclear ?-catenin decreased after starting the invasive neoplastic process. This suggests a role for this protein in the progression of dysplasia and early malignant transformation to OSCC. Immunodetection of ?-catenin could be a possible immune marker in the detection of oral dysplasia. Key words:Oral squamous cell carcinoma (OSCC), ?-catenin, oral dysplasia.
Highlights
Oral Squamous Cell Carcinoma (OSCC) is the most common malignancy of the oral cavity, and its early diagnosis is essential to improve patient survival and significantly reduce mortality rates [1]
Some studies have been undertaken to try to determine whether the expression of Ki-67 antigen is related to the presence of epithelial dysplasia [21], since the increase in cell proliferation is considered to be feature for malignant progression [22,23]
Zoeller et al, [9] studying epithelial dysplasia observed that the percentage of cells expressing Ki-67 increases according to the histopathologic malignancy degree
Summary
Oral Squamous Cell Carcinoma (OSCC) is the most common malignancy of the oral cavity, and its early diagnosis is essential to improve patient survival and significantly reduce mortality rates [1]. Inhibition of β-catenin degradation caused by Wnt ligand results in the accumulation of this cytoplasmic protein and subsequent translocation to the nucleus, forming a complex with Lymphoid Stimulating Factor-1/T cell Factor (LEF-1/ TCF) that displaces protein Groucho and assumes the function of co-activator, inducing transcription of target genes of Wnt signaling pathway, associated with cell growth and proliferation [17,18] If this route presents changes its performance it can lead to uncontrolled cell growth and tumor formation. -2.3 Immunohistochemical evaluation of β-catenin In all samples of normal oral mucosa epithelium, localization of β-catenin was detected in the cell membrane and there was negative immunostaining at cytoplasm and/or nuclear level.
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