# E-Cadherin Immunohistochemical Expression in Gastrointestinal Adenocarcinomas and Its Association With Histological and Prognostic Parameters

**Authors:** Sarumathi Varadan, Uma Balasundararajan, Dhivya Manoharan, Balaji S Mahendran

PMC · DOI: 10.7759/cureus.101801 · Cureus · 2026-01-18

## TL;DR

This study shows that reduced E-cadherin expression in gastrointestinal cancers is linked to more aggressive tumor features and worse outcomes.

## Contribution

The study introduces a semi-quantitative scoring system for E-cadherin expression and demonstrates its prognostic relevance in GI adenocarcinomas.

## Key findings

- Reduced or absent E-cadherin expression is strongly associated with poorly differentiated and infiltrating tumor types.
- Loss of E-cadherin correlates with advanced tumor stage, higher nodal metastasis, and perineural invasion.
- Well-differentiated tumors and intestinal-type adenocarcinomas retain E-cadherin expression.

## Abstract

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.

## Linked entities

- **Genes:** CDH1 (cadherin 1) [NCBI Gene 999]
- **Proteins:** shg (shotgun)
- **Diseases:** gastric adenocarcinoma (MONDO:0005036), colonic adenocarcinoma (MONDO:0002271), rectal adenocarcinoma (MONDO:0002169)

## Full-text entities

- **Genes:** TENM1 (teneurin transmembrane protein 1) [NCBI Gene 10178] {aka ODZ1, ODZ3, TEN-M1, TEN1, TNM, TNM1}, ITK (IL2 inducible T cell kinase) [NCBI Gene 3702] {aka EMT, LPFS1, LYK, PSCTK2}, CTNND1 (catenin delta 1) [NCBI Gene 1500] {aka BCDS2, CAS, CTNND, P120CAS, P120CTN, p120}, SNAI1 (snail family transcriptional repressor 1) [NCBI Gene 6615] {aka SLUGH2, SNA, SNAH, SNAIL, SNAIL1, dJ710H13.1}, CDH1 (cadherin 1) [NCBI Gene 999] {aka Arc-1, BCDS1, CD324, CDHE, ECAD, LCAM}, CTNNB1 (catenin beta 1) [NCBI Gene 1499] {aka CTNNB, EVR7, MRD19, NEDSDV, armadillo}, SNAI2 (snail family transcriptional repressor 2) [NCBI Gene 6591] {aka SLUG, SLUGH, SLUGH1, SNAIL2, WS2D}
- **Diseases:** gastrointestinal carcinogenesis (MESH:D063646), Diffuse gastric cancer (MESH:D013274), Colon tumors (MESH:D003110), MERS (MESH:D015161), , and rectum (MESH:D012004), intestinal-type cancers (MESH:D007414), Tumors (MESH:D009369), Adenocarcinoma NOS (MESH:D000230), Gastrointestinal (GI) cancers (MESH:D005770), lymph node metastasis (MESH:D008207), gastric (MESH:D013272), Breast ductal carcinoma (MESH:D018270), colon (MESH:D003108), signet (MESH:D018279), colorectal cancer (MESH:D015179), NOS (MESH:C536665), Nodal metastasis (MESH:D009362), nodal (MESH:D013611), mucinous (MESH:D002288)
- **Chemicals:** TBS (MESH:D013725), water (MESH:D014867), paraffin (MESH:D010232), EDTA (MESH:D004492), xylene (MESH:D014992), calcium (MESH:D002118), Formalin (MESH:D005557), alcohol (MESH:D000438), Eosin (MESH:D004801), 3,3'-diaminobenzidine (MESH:D015100), PBS (MESH:D007854), Hematoxylin (MESH:D006416), H&amp;E (MESH:D006371), hydrogen peroxide (MESH:D006861), PolyExcel (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

26 references — full list in the complete paper: https://tomesphere.com/paper/PMC12912817/full.md

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Source: https://tomesphere.com/paper/PMC12912817