Overexpression of LI-cadherin in gastric cancer is associated with lymph node metastasis

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Abstract

Gastric cancer remains the second leading cause of cancer deaths worldwide. Patients usually present late with local invasion or metastatic diseases. The present study investigated the expression level of liver-intestine cadherin (LI-cadherin) by RT-PCR and its correlation with clinicopathological data in 71 pairs of tumor and non-cancerous gastric mucosa. Protein expression level of LI-cadherin was determined by Western blotting and immunohistochemistry. The mRNA of LI-cadherin was highly expressed in tumor as compared to non-cancerous mucosa. Lymph node metastasis was significantly associated with the expression of LI-cadherin (p=0.038). On multivariate analysis, T staging and LI-cadherin expression were found to be independent factors associated with lymph node metastasis.

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Materials and methods

Patients and specimens. Seventy-one pairs of tumor and non-cancerous gastric mucosa were obtained from patients who underwent gastrectomy for histologically proven gastric adenocarcinoma at the University of Hong Kong Medical Center, Queen Mary Hospital, from October 2001 to April 2003. Metastatic lymph nodes were also harvested during gastrectomy. Immediately after removal, the tissues were split into two parts, one snap-frozen in liquid nitrogen and stored at −80 °C until use, and the other

Clinicopathological data (Table 1)

There was a slight male predominance. The majority of tumors were located in the distal stomach (65%) and of intestinal type (61%) according to Lauren’s classification [9]. The tumors were staged according to the criteria of the Japanese Research Society for Gastric Cancer [10]. Most patients presented late with advanced diseases as evidenced by their advanced stages and high incidence of lymph node metastasis (Table 1).

Over-expression of LI-cadherin mRNA

LI-cadherin was absent in half of the non-cancerous mucosal specimens but

Discussion

The exact mechanism responsible for the development of gastric cancer is still unclear. A number of studies have shown that the development of gastric cancer is a multi-step process that involves changes in multiple genes including tumor suppressor genes, oncogenes, cell cycle regulators, growth factors, and cell adhesion molecules [11]. Chromosomal abnormalities such as microsatellite instability [12], loss of heterozygosity [13], and point mutations of the p53 gene [14] are often found in

Acknowledgements

This study was partly supported by a grant from the Research Grants Council (RGC) of the Hong Kong Special Administrative Region, China (Project No. HKU 7247/99M), as well as by the Gastric Cancer Research Fund of the Department of Surgery, University of Hong Kong Medical Center. We thank Dr. Z. Li for advice in immunohistochemical results. We are grateful to P.Y. Lee for advice in statistical analysis. We also thank M.X. Zhou, A.O. Chan, and L.L. Shing for technical assistance.

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