The expression of E-cadherin and cathepsin-D in normal oral mucosa, oral epithelial dysplasia and oral squamous cell carcinoma: A comparative analysis between immunohistochemistry and routine histopathology

• Published in: Journal of oral and maxillofacial pathology : JOMFP 2011-09, Vol.15 (3), p.288-294
• Main Authors: Yogesh, Tl, Narayan, Tv, Shreedhar, Balasundari, Shashidara, R, Leekymohanty
• Format: Article
• Language: English
• Subjects: Cell adhesion & migration; Drinking water; Original; Proteins; Statistical methods
• ISSN: 0973-029X; 1998-393X
• DOI: 10.4103/0973-029X.86689

E-cadherin is known to be an invasion suppressor gene and cathepsin-D, a protease, which is an invasion promoter and plays a central role in solid tumors including oral cancer. To look for the expression pattern in normal buccal mucosa, dysplastic oral epithelium and oral squamous cell carcinoma (SCC) along with their correlation to individual atypical features, thereby providing an objective to the grading system in predicting the fate of affected epithelium. To elucidate the expression patterns of these markers, we examined immunohistochemically on formalin fixed, paraffin embedded sections 22 dysplastic epithelia, eight SCC and ten normal buccal mucosa. In dysplastic epithelium slight loss of expression of E-cadherin was noted as grade of dysplasia increased. Two cases of carcinoma clearance showed only basal and suprabasal staining. The staining varied in SCC with patchy to complete absence of expression. With cathepsin-D fine to moderate granular cytoplasmic staining was noted in most of the dysplastic epithelium. Similar staining was noted in SCC. The atypical features which strongly correlated to loss of expression of E-cadherin and intense cathepsin-D expression are basilar hyperplasia, loss of cohesion, mitosis, loss of polarity and drop shaped rete ridges. The result of the study shows that the above atypical features should be given more weightage in addition to traditional grading system, in predicting the fate of affected epithelium. Additional studies with larger sample size and using monoclonal antibody against cathepsin-D may further strengthen our findings.