Biological implications of circulating soluble intercellular adhesion molecule-1 in colorectal cancer patients

被引:14
|
作者
Araki, T [1 ]
Miki, C [1 ]
Kusunoki, M [1 ]
机构
[1] Mie Univ, Sch Med, Dept Surg 2, Tsu, Mie 5148507, Japan
关键词
colon cancer; immune suppression; intercellular adhesion molecule; metastasis;
D O I
10.1080/003655201300051234
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background: Intercellular adhesion molecule-1 (ICAM-1) is assumed to play a role in cell-cell and cell-extracellular matrix interactions. We evaluated the relationship between local expression of ICAM-1 and the circulating level of sICAM-1, and clarified its biological implications. Methods: Serum concentrations of sICAM-1 in 94 colorectal cancer patients were determined. Tissue concentrations of sICAM-1 in the tumor, colorectal adenoma, and the normal mucosa were also determined. The expression of ICAM-1 in the tumor was evaluated immunohistochemically. Results: The serum concentration of sICAM-1 in the patients was significantly higher than that in the controls, and the tumor size was the independent pathological factor that was associated with the serum ICAM-1 level. ICAM-1 immunoreactivity was seen intensively in the stromal cells in the tumor. The tissue concentration of sICAM-1 in the normal mucosa was significantly lower than that in the adenoma and the early carcinoma. The tissue concentration of sICAM-1 in the advanced carcinoma significantly decreased in association with the increase in tumor size. This fluctuation of ICAM-1 expression in the tumor was also associated with the metastatic potential even at an early stage of the disease. Conclusions: The tissue concentration of sICAM-1 increased during tumorigenesis and at an early stage of carcinoma, and decreased in association with progression of the disease. Serum sICAM-1 level reflected the fluctuation of ICAM-1 expression in the tumor. Evaluation of serum concentration of sICAM-1 may be associated with tumor load and can reflect disease progression in colorectal cancer patients.
引用
收藏
页码:399 / 404
页数:6
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