| Project/Area Number |
15K19537
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Endocrinology
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| Research Institution | Toho University (2017)
National Cancer Center Japan (2015-2016) |
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Principal Investigator |
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| Research Collaborator |
OHKI Rieko 国立がん研究センター, 基礎腫瘍学ユニット, 主任研究員
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | p53 / Akt / 神経内分泌腫瘍 / PHLDA3 |
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| Outline of Final Research Achievements |
PHLDA3 functions as a tumor suppressor gene through suppression of Akt in the neuroendocrine tumors (NETs) of lung and pancreas. PHLDA3 gene-deficient mice show abnormality of endocrine tissue such as hyperplasia of pancreatic islets. For these reasons, it is considered that PHLDA3 is important for suppression of NETs occurring in various organs. Therefore, we investigated the importance of PHLDA3 gene in gastrointestinal neuroendocrine tumor (GI-NET) by collecting GI-NET specimens followed by LOH analysis of PHLDA3 gene. In addition, it was revealed that PHLDA3 deficiency improves islets engraftment through the suppression of apoptosis caused by hypoxic damage (PLOS ONE, 2017).
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