Journal
HUMAN PATHOLOGY
Volume 43, Issue 7, Pages 1094-1102Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.humpath.2011.08.020
Keywords
Serrated adenocarcinoma; E-cadherin; beta-Catenin; Laminin 5 gamma 2; Cell adhesion
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Funding
- Instituto de Salud Carlos III, Ministerio de Sanidad, Madrid, Spain [P1081210]
- Academy of Finland, Helsinki, Finland [127990]
- Academy of Finland (AKA) [127990, 127990] Funding Source: Academy of Finland (AKA)
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The immunohistochemical expression of cell adhesion molecules in colorectal serrated adenocarcinoma is still unknown. The immunostaining patterns of beta-catenin, E-cadherin, P-cadherin, laminin 5 gamma 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 beta-catenin, membranous E-cadherin, and nuclear SMAD4 but an increased cytoplasmic expression of laminin-5 gamma 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 beta-catenin in SAC, especially in right-sided tumors, suggests that molecular mechanisms other than the canonical Wnt/beta-catenin pathway may have a role in tumor bud formation. (C) 2012 Elsevier Inc. All rights reserved.
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