| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2003: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Research Abstract |
We assume that EBV has a role in the immortalization of gastric epithelial cells near the atrophic border during the course of chronic atrophic gastritis, when atrophy in the area of the fundic glands has advanced a moderate degree,. However, tests used in the past have limitations in sensitivity or specificity, such that it is difficult to evaluate in detail the degree or distribution of EBV infection in the gastric mucosa of chronic atrophic gastritis, which is the origin of gastric cancer.
In this study, we investigated the appearance of EBV in relation to : The stage of chronic gastritis at which it appeared ; the area of the stomach ; the amount (copy number) ; and the infectious condition. In addition, we studied the contribution of EBV to the development of gastric cancer.
Initially, in order to investigate the origin of the EBV- associated gastric cancer, immunohistochemistry of mucus was performed to determine the mucus type of the tumor (gastric type, intestinal type). EBV dete
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ction, immunohistochemistry to determine the mucus type (human gastric mucin, muc2, CD10), and PAS alcian blue staining were performed on 120 cases with gastric cancer that were diagnosed and treated at our hospital. The mucus type of EBV-associated gastric cancer that was advanced and required surgery was the gastric type.
EBV is detected in 30% of remnant gastric carcinomas. Therefore, we evaluated the background gastric mucosa of EBV-positive gastric remnant carcinomas, which was frequently found at the anastomotic site created by the Billroth-2 method and was mainly a depressed type of advanced cancer. The background gastric mucosa frequently showed intestinal metaplasia, but it rarely occurred together with gastric cystic polyposis (CCP).
Because a relationship between H. pylori and gastric cancer has been noted, we evaluated the communication between EBV and H. pylori using EBV-infected cultured cells and monitoring cytokine production. We observed that IL-8 production by EBV-infected cultured cells increased with H. pylori stimulation. Less
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