ICAM‐1 expression and the soluble ICAM‐1 level for evaluating the metastatic potential of gastric cancer

ICAM‐1 plays an important role in cell–cell and cell–extracellular matrix interactions, especially tumor invasion and cytotoxicity of lymphocytes. In the present study, the relationship between metastasis of gastric cancer and ICAM‐1 expression by cancer cells or the serum level of s‐ICAM‐1 was (s‐I...

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Published inInternational journal of cancer Vol. 100; no. 4; pp. 486 - 490
Main Authors Maruo, Yukinobu, Gochi, Akira, Kaihara, Akihiko, Shimamura, Hiroshi, Yamada, Takatoshi, Tanaka, Noriaki, Orita, Kunzo
Format Journal Article
LanguageEnglish
Published New York Wiley Subscription Services, Inc., A Wiley Company 01.08.2002
Wiley-Liss
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Summary:ICAM‐1 plays an important role in cell–cell and cell–extracellular matrix interactions, especially tumor invasion and cytotoxicity of lymphocytes. In the present study, the relationship between metastasis of gastric cancer and ICAM‐1 expression by cancer cells or the serum level of s‐ICAM‐1 was (s‐ICAM‐1) was examined. ICAM‐1 was detected by immunohistochemic staining in 49.0% of 108 patients with gastric cancer. The ICAM‐1 expression rate was higher at a more advanced stage, based on lymph node metastasis, being 46.9% in node‐negative and 56.1% in node‐positive cases. In patients with liver metastasis, the rate was 90.9%, while it was 43.3% in patients without liver metastasis (p < 0.05). The serum s‐ICAM‐1 level was 262.1 ng/ml (median 205.5, range 176.0–271.0) in healthy subjects and 391.5 ng/ml (median 317.5, range 148.7–1,768.0) in gastric cancer patients (p < 0.001). The serum s‐ICAM‐1 level was significantly higher in patients with liver metastasis than in patients without liver metastasis (p < 0.0001). In addition, positive ICAM‐1 expression cases had significantly higher s‐ICAM‐1 levels than negative ones, 408.9 ± 188.4 and 308.1 ± 88.1 ng/ml, respectively. These results suggested that ICAM‐1 was overexpressed in cancer cells and released as s‐ICAM‐1, which would promote hematogenous metastasis by suppressing local anticancer immunity. © 2002 Wiley‐Liss, Inc.
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ObjectType-Article-1
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ISSN:0020-7136
1097-0215
DOI:10.1002/ijc.10514