The significance of beta-catenin, E-cadherin, and P-cadherin expressions in neoplastic progression of colorectal mucosa : an immunohistochemical study

Background and study aims : The purpose of the current study was to investigate the role of b-catenin, E-cadherin and P-cadherin in colorectal carcinogenesis using tissue array method. Patients and methods : Core tissue biopsies were taken from paraffin-embedded tissue blocks of 167 cases including 26 normal mucosae (NM), 99 colorectal polyps (10 hyperplastic polyps (HP), 8 traditional serrated (TSA), 17 tubular (TA), 37 tubulovillous (TVA), and 27 villous adenomas (VA)), 14 adenomas with intra- mucosal carcinoma (ACA), and 28 colorectal cancers (CCA). Immunohistochemistry was performed using antibodies to b- catenin, E-cadherin, and P-cadherin. Distribution of positivity was assessed using percentage expression while an arbitrary grading scale was used for staining intensity. Results : b-catenin expression was cytoplasmic, membranous, and nuclear. Both E-cadherin and P-cadherin expressions were confined to cytoplasmic-membranous compartments. Membranous expression of b-catenin significantly decreased in CCA (p < 0.01). Nuclear b-catenin expression significantly increased in close correlation with neoplastic sequence reaching its highest expression in ACA and CCA (p < 0.001). Polyps with intraepithelial neoplasia (IEN) showed significantly higher nuclear b-catenin expression in parallel with increasing grades of IEN (p < 0.001). E-cadherin and P-cadherin expression increased in polyps, whereas a significant decrease in their expression was observed in CCA (p < 0.001) while E-cadherin expression signifi- cantly increased in CCA compared to NM (p < 0.001), no such difference was observed in P-cadherin expression. Conclusions : Nuclear b-catenin expression correlating with the grade of IEN in polyps and carcinomas supports its role in colo- rectal carcinogenesis. E-cadherin and P-cadherin expressions in adenomas suggest that these molecules might have role in adeno- ma formation though not necessarily be involved in neoplastic progression. (Acta gastroenterol. belg., 2007, 70, 339-344).