The relationship between expression of ICAM-1 and VEGF-D in gastric cancer and its significance
10.3781/j.issn.1000-7431.2008.10.013
- Author:
Ming-Yi ZHANG
1
Author Information
1. Department of General Surgery
- Publication Type:Journal Article
- Keywords:
Cell adhesion molecules;
Lymphatic metastasis;
Stomach neoplasms;
Vescular endothelial growth factor
- From:
Tumor
2008;28(10):873-876
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the relationship between intercellular adhesion molecule-1 (ICAM-1) and the signaling pathway of vascular endothelial growth factor receptor-3 (VEGFR-3) in gastric cancer and explore the mechanism underlying the lymphatic metastasis of gastric cancer. Methods: Totally 100 grastic cancer patients were recruited in the study including 13 cases of early gastric cancer and 87 cases of advanced gastric cancer with lymphatic metastasis (50 cases) and without lymphatic metastasis (37 cases). Thirty cases of normal gastric mucosa in the distance of > 5 cm from gastric cancer lesions were used as controls. The expressions of VEGF-C, VEGF-D, VEGFR-3, ICAM-1 and lymphatic microvessel density (LMVD) were detected using immunobistochemical method (EnVision™). The lymphatic and vascular invasions of gastric cancer were observed by microscopy. Results: The positive expression rate of ICAM-1 was increased with The increase in infiltration depth. It was 0% in the control, 7.7% in early stage gastric cancer, and 31.0% in advanced gastric cancer, respectively (P < 0.05). The positive rate of ICAM-1 expression was related with lymphatic metastasis (P < 0.005), depth of tumor invasion (P < 0.025), VEGF-C expression (P < 0.025), and VEGF-D expression (P < 0.005). Logistic regression analysis showed that the positive expression of ICAM-1 correlated with lymph node metastasis and expression of VEGF-D (P = 0.001 2, P = 0.023 7). Conclusion: ICAM-1 expression has positive correlation with expression of VEGF-D. The mechanism may be contributed to regulation of ICAM-1 expression by VEGF-D via VEGFR-2 signaling pathway.
