Journal of Baghdad College of Dentistry (Sep 2016)
β- catenin Expression and Its Relation to Bryne’s Invasive Grading System in Oral Squamous Cell Carcinoma
Abstract
Background: Invasion in oral cancer involves alterations in cell-cell and cell-matrix interactions that accompanied by loss of cell adhesion. Catenins stabilize cellular adherence junctions by binding to E-cadherin, which further mediates cell-cell adhesion and regulates proliferation and differentiation of epithelial cells. The Wnt/β-catenin pathway is one of the major signaling pathways in cell proliferation, oncogenesis, and epithelial-mesenchymal transition. Aims of the study: to detect immunohistochemical distribution pattern and different subcellular localization of β-catenin in oral squamous cell carcinoma and relate such expression to Bryne’s invasive grading system. Materials and Methods: This study included 30 paraffin blocks of primary oral squamous cell carcinoma. Bryne’s grading performed on routein stained slides. Immunohistochemical staining for anti β-catenin was done to illustrate its pattern and subcellular localization in malignant cells. The expression correlated with the invasive grading system. Results: β-catenin expression detected in all sample (100%). It was (23.3%) membranous, (60%) aberrant cytoplasmic and (16.7%) mixed expression. Diffuse strong homogeneous pattern was observed in (40%) of the cases. The cytoplasmic expression had significant high mean rank in score 3, diffuse strong homogeneous pattern and strong intensity. Well-differentiated carcinoma expressed great mixed membranous/cytoplasmic expression while poor-differentiated cases showed low membranous mean rank expression. The strong diffuse homogeneous pattern with strong staining was significantly frequent in well-differentiated squamous cell carcinoma. Conclusion: Increase cytoplasmic β-catenin expression is parallel with carcinoma dedifferentiation. Suggesting maintenance of its adhesive role with the inhibition of the normal degradation of free β-catenin in the cytoplasm, which might cause accelerated tumor cell proliferation.