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The novel mechanism of hematologic malignancy through epigenetic abnormality caused by iron overload

Research Project

Project/Area Number 15K18394
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Tumor biology
Research InstitutionAsahikawa Medical College

Principal Investigator

Yamamoto Masayo  旭川医科大学, 大学病院, 医員 (30596284)

Research Collaborator TANAKA Hiroki  
Project Period (FY) 2015-04-01 – 2018-03-31
Project Status Completed (Fiscal Year 2017)
Budget Amount *help
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Keywords鉄過剰 / エピジェネティクス / DNAメチル化 / 糖代謝
Outline of Final Research Achievements

In the study, we found that the enzymes associated with glucose metabolism were increased in the iron overloaded mice that received short-term iron overload. Furthermore, 2-hydroxyglutarate (2-HG), which was aberrant metabolites in the TCA cycle, was increased in the iron overloaded mice. Furthermore, the 2-HG production resulted in upregulation of DNA methylation in the iron overloaded mice. From these results, we considered that DNA methylation were increased by iron overload through enhancement of the abnormal glucose metabolism.
On the other hands, when we performed similar analysis using long-term iron overload model mice, DNA methylation were rather decreased in the iron overloaded mice. To know the detailed mechanism during iron overload, we need further analysis by focusing the period of iron overload.

Report

(4 results)
  • 2017 Annual Research Report   Final Research Report ( PDF )
  • 2016 Research-status Report
  • 2015 Research-status Report

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Published: 2015-04-16   Modified: 2019-03-29  

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