| Project/Area Number |
14570437
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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 |
Gastroenterology
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
SUGIYAMA Toshiro Hokkaido University, Graduate School of Medicine, Prof., 大学院・医学研究科, 助教授 (00196768)
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| Co-Investigator(Kenkyū-buntansha) |
ASAKA Masahiro Hokkaido University, Graduate School of Medicine, Prof., 大学院・医学研究科, 教授 (10113507)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2003: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2002: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | H.pylon / Gastric MALT lymphoma / API2-MALT1 chimeric transcript / NF-kB activation / NF-κB / アポトーシス |
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| Research Abstract |
Total gastrectomy was an established conventional treatment against gastric MALT lymphoma. As the 60-80% of gastric MALT lymphoma regress by an eradication treatment of H.pylon and the remaining 20-40% does not, the predictive factor to eradication treatment should be clinically identified. The translocation between API2 gene in Ch11 and MALT1 gene in Ch18 was observed in a part of gastric MALT lymphoma and the high sensitive detection method of the chimeric transcript was established By using this system, the presence of API2-MALT1 chimeric transcript was an important predictive factor to resist for eradication treatment. These results suggest us that the presence of API2-MALT1 chimeric transcript might have a causal linkage to occurrence of eradication-resistant gastric MALT lymphoma. The transfection of API2-MALT1 chimeric cDNA into COS7 cells have induced an accumulation of the chimeric protein within the cytoplasm and demonstrated the delayed degradation of the protein. The accumulation of the chimeric protein within the cytoplasm resulted in an activation of NF-kB in the nucleus. Therefore, the presence of API2-MALT1 chimenc transcript might have a causal linkage to tumorgenesis via NF-kB activation in eradication-resistant gastric MALT lymphoma.
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