β-catenin expression and its relation to bryne’s invasive grading system in oral squamous cell carcinoma

الملخص EN

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 poordifferentiated 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