Immunohistochemical expression profile of β -catenin, E-cadherin, P-cadherin, laminin-5 γ 2 chain, and SMAD4 in colorectal serrated adenocarcinoma

• Published in: Human pathology Vol. 43; no. 7; pp. 1094 - 1102
• Main Authors: García-Solano, José, MD, Conesa-Zamora, Pablo, PhD, Trujillo-Santos, Javier, MD, PhD, Torres-Moreno, Daniel, D, BSc, Mäkinen, Markus J., MD, PhD, Pérez-Guillermo, Miguel, MD, PhD, FIAC
• Format: Journal Article
• Language: English
• Published: 2012
• Subjects: Pathology; Laminin 5 γ2; Cell adhesion; Serrated adenocarcinoma; β-Catenin; E-cadherin
• ISSN: 0046-8177; 1532-8392
• DOI: 10.1016/j.humpath.2011.08.020

Summary The immunohistochemical expression of cell adhesion molecules in colorectal serrated adenocarcinoma is still unknown. The immunostaining patterns of β -catenin, E-cadherin, P-cadherin, laminin 5 γ 2, and SMAD4 and their relationship to survival were studied in different tumor areas, namely, tumor center and invasive front, the latter comprising tumor bud and non–tumor bud clusters, as described in a previous study of 66 serrated adenocarcinomas and matched conventional carcinomas. Compared with conventional carcinomas, serrated adenocarcinomas showed significantly reduced nuclear β -catenin, membranous E-cadherin, and nuclear SMAD4 but an increased cytoplasmic expression of laminin-5 γ 2 at the invasive front that was particularly pronounced in the tumor buds. E-cadherin loss at the invasive front was identified as an independent prognostic factor for a poorer outcome in serrated adenocarcinoma. Serrated adenocarcinoma shows a distinct immunohistochemical profile at the invasive front compared with conventional carcinoma, which may account for its less favorable outcome. The lower frequency of nuclear β -catenin in SAC, especially in right-sided tumors, suggests that molecular mechanisms other than the canonical Wnt/ β -catenin pathway may have a role in tumor bud formation.