1999 Fiscal Year Final Research Report Summary
Stimulation of Cancer Metastases in Systemic Inflammatory Response Syndrome
| Project/Area Number |
10671124
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Kumamoto University |
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Principal Investigator |
HIROTA Masahiko Kumamoto University School of Medicine Assisstant, 医学部・附属病院, 助手 (80284769)
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| Co-Investigator(Kenkyū-buntansha) |
MITA Seiji Kumamoto University School of Medicine Assisstant, 医学部・附属病院, 助手 (10671125)
OGAWA Michio Kumamoto University School of Medicine Professor, 医学部, 教授 (30028691)
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| Project Period (FY) |
1998 – 1999
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| Keywords | pancreatic cancer / SIRS / metastasis / TNF α / E-selectin / sialyl Lewis^a / no-touch isolation / 手術侵襲 |
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| Research Abstract |
We studied the effect of tumor necrosis factor α (TNF α), one of the major inflammatory cytokines, on the adhesive reaction of pancreatic cancer cells to human umbilical vein endothelial cells (HUVECs) and on the hepatic metastasis of cancer cells in vivo. After TNF α stimulation, the expression of E-selectin, an adhesion molecule to neutrophils on HUVECs, increased. In addition, the adhesion of pancreatic cancer cells to HUVECs increased after TNF α stimulation, as was observed with neutrophils. The TNF α-induced adhesive response depended on the extent of sialyl Lewis^a expression on cancer cells. The hepatic metastasis in vivo was often observed when cancer cells expressing a high amount of sialyl Lewis^a were inoculated intrasplenically after increase in plasma TNF α concentration. Because sialyl Lewis^a on cancer cells is a ligand for E-selectin, as sialyl Lewis^x on neutrophils, TNF α upregulated the adhesion between sialyl Lewis^a on cancer cells and E-selectin on HUVECs. These results suggest that production of TNF α after surgical trauma may stimulate the metastasis of cancer cells with high sialyl Lewis^a expression.
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