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Published on: July 20, 2014
E-Cadherin Immunohistochemical Expression in Gastrointestinal Adenocarcinomas and Its Association With Histological
Sarumathi Varadan1, Uma Balasundararajan1, Dhivya Manoharan2
1Department of Pathology, Indira Medical College and Hospital, Thiruvallur, IND.
Background:
E-cadherin (CDH1) is a critical cell adhesion molecule that maintains epithelial tissue integrity. Its loss or dysfunction is a hallmark of the epithelial-mesenchymal transition (EMT) and is mostly implicated in gastrointestinal adenocarcinomas, their invasion, and metastasis.
Objectives:
This study aims to evaluate the patterns of E-cadherin immunohistochemical expression in gastrointestinal (GI) adenocarcinomas using a semi-quantitative scoring system and to correlate these patterns with the histological and prognostic factors of tumors.
Methods:
This prospective and retrospective observational study included 50 patients diagnosed with GI adenocarcinoma (stomach, colon, and rectum) at a tertiary care center. Immunohistochemistry (IHC) for E-cadherin was performed on formalin-fixed paraffin-embedded tissue, and the expression of E-cadherin was evaluated using the Jawhari et al. scoring system. Statistical associations between expression patterns and clinicopathological variables were analyzed using the chi-square test, with a p-value < 0.05 considered significant.
Results:
The study population (N=50) comprised 21 gastric (42%), 10 colonic (20%), and 19 rectal adenocarcinomas (38%). Reduced or absent staining of E-cadherin (score 0 - 1) was seen in 19 (38%) of GI adenocarcinomas, and 14 (28%) tumors showed completely preserved E-cadherin expression (score 3). Well-differentiated tumors showed preserved E-cadherin expression (scores 2-3 in all cases), whereas poorly differentiated tumors predominantly showed reduced or complete loss of expression (p=0.001). Adenocarcinoma NOS and intestinal-type tumors largely retained E-cadherin, while signet ring cell, mucinous, and infiltrating types frequently demonstrated markedly decreased expression (p=0.001). No statistically significant association was observed between tumor site and E-cadherin expression. Reduced or absent E-cadherin expression was significantly associated with advanced tumor stage (p=0.002), higher nodal stage (p=0.018), and perineural invasion (p=0.008).
Conclusion:
E-cadherin dysregulation is strongly associated with histological tumor grade, adenocarcinoma type, tumor stage, nodal metastasis, and perineural invasion in GI adenocarcinomas. The significant loss of expression in poorly differentiated and infiltrating tumor types supports its role as an invasion suppressor. Loss of E-cadherin expression in advanced tumor stages, higher nodal metastasis, and perineural invasion elucidate the role of E-cadherin as a useful prognostic immunohistochemical marker in gastrointestinal adenocarcinomas.
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