| Project/Area Number |
11671278
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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 |
Digestive surgery
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| Research Institution | TOKAI UNIVERSITY |
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Principal Investigator |
OGOSHI Kyoji (2000-2001) TOKAI UNIVERSITY, DEPT OF SURGERY, ASSOCIATE PROFESSOR, 医学部, 助教授 (30112775)
宮治 正雄 (1999) 東海大学, 医学部, 助手 (90219783)
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| Co-Investigator(Kenkyū-buntansha) |
生越 喬ニ 東海大学, 医学部, 助教授 (30112775)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2001: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2000: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1999: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | gastrin / gastrin receptor / gastric cancer / cytokine / G-cell / IL-1 β / TNF-α / IL-8 / pepsinogen / サイトカイン / 炎症性サイトカイン / ガストリン / G細胞 / ガストリン受容体 / 胃癌 |
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| Research Abstract |
Under this Grant in Aid for Scientific Research, we have clinically confirmed as follows, 1) The initiation and proliferation in early gastric cancer were affected by the environment of hypergastrinemia in aging. 2) The prognosis of patients with hypergastrinemia was significantly worse than those with low gastrinemia, especially in the patients with poorly differentiated gastric cancer. 3) The expression of c-erbB-2, EGFR, PCNA and Ki-67 in the patients with hypergastrinemia were significantly more frequently than those with low gastrinemia. Furthermore, we evaluated whether or not the expression of gastrin receptor gene exists in gastric cancer by using RT-PCR method, and as a result the expression rate of the gene was 10.6% (5/47). We speculated that the expression of the receptor affected either tumor proliferation or metastasis from the clinicopathological examination. Finally, after we established the system of G-cells primary culture from guinea-pig's stomach, we found the inflammatory cytokines, such as IL-1β, TNF-α and IL-8, stimulated gastrin production and secretion from G-cells. These results suggest that endogenous hypergastrinemia may play an important role in pathophysiology of gastric cancer.
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