, Volume 58, Issue 3, pp 699-705,
Open Access This content is freely available online to anyone, anywhere at any time.
Date: 04 Oct 2012

Liver–Intestine-Cadherin Is a Sensitive Marker of Intestinal Differentiation During Barrett’s Carcinogenesis

Abstract

Background

Histopathologic differentiation between the stages of Barrett’s carcinogenesis is often challenging. Liver–intestine (LI)-cadherin, an intestine-specific marker, is involved in intestinal metaplasia development in gastric and colon cancers and could be of value in diagnosis and differentiation.

Aims

To examine the expression of LI-cadherin in the sequence of Barrett’s carcinogenesis and to evaluate its association with clinicopathological data.

Methods

LI-cadherin expression was immunohistologically investigated, by use of anti-CDH17 antibody, in gastric mucosa (GM) biopsies taken from the cardia (n = 9), in Barrett’s esophagus (BE) without intraepithelial neoplasia (without IEN) (n = 9) and BE with low-grade IEN (n = 11), and in esophageal adenocarcinoma (ADC) (n = 13).

Results

The immunoreactivity score was highest in adenocarcinoma (mean IRS = 4.0), and dropped gradually from BE with IEN and BE without IEN (mean IRS = 2.0) to cardia mucosa (IRS = 0). Similarly, the intensity of staining and the percentage of positive cells increased during the sequential stages of BE carcinogenesis. Comparative analysis showed that LI-cadherin expression was significantly different between cardiac epithelium and ADC. Also, percentage of positive cells in GM was significantly different from that in BE with IEN. LI-cadherin IRS was lower for tumors with poor differentiation than for moderately differentiated tumors, but the difference was not statistically significant.

Conclusions

LI-cadherin is a sensitive marker of intestinal metaplasia and can be helpful for early histologic diagnosis of Barrett’s esophagus; it is, however, not significantly different between BE with and without IEN, and cannot be used to distinguish between these.

Anna Mokrowiecka and Sarah Zonnur contributed equally to this work.