2015 Fiscal Year Final Research Report
Analysis of the higher-order regulatory mechanism of LT-beta epigenome, leading to clinical application.
Project/Area Number |
25860543
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Gastroenterology
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Research Institution | Kumamoto University |
Principal Investigator |
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Project Period (FY) |
2013-04-01 – 2016-03-31
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Keywords | LTβ / NF-κB / CTCF / epigenetics / exosome |
Outline of Final Research Achievements |
Using the hepatic cell-line which NF-κB signal was activated constitutively, we showed that constant activation of NF-κB was important to activation of LTβ. In addition, we found the possibility of NF-κB as one of personalized medicine for the LT β overexpression group, because the expression of LTβ was controlled by NF-κB inhibitor. ・An tissue examination was necessary to confirm LTβ expression, conventionally. We found that LTβ in serum exosome could be detected quantitatively. We also found LTβ expression in the liver cancer tissue was in proportion to LTβ in serum exosome. In addition, the group highly expressed LTβ in exosome had a poorer prognosis than low expression group.
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Free Research Field |
消化器内科
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