| Project/Area Number |
26460413
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Human pathology
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| Research Institution | Tohoku University |
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Principal Investigator |
KASAJIMA ATSUKO 東北大学, 医学系研究科, 大学院非常勤講師 (50623005)
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| Co-Investigator(Renkei-kenkyūsha) |
SASANO Hironobu 東北大学, 医学系研究科, 教授 (50187142)
NAKAMURA Yasuhiro 東北医科薬科大学, 医学部, 教授 (80396499)
MIKI Yasuhiro 東北大学, 災害科学国際研究所, 講師 (50451521)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 神経内分泌腫瘍 / 内分泌腫瘍 / Neuroendocrine tumor / Progesteron receptor / Cell cycle |
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| Outline of Final Research Achievements |
Progesteron receptor: PR is frequently expressed in pancreatic neuroendocrine tumor: PNET and is related to a longer prognosis of the patients. However, its mechanism is not clarified. Expression of PR subtype A (PRA) was negatively associated with multiple cell cycle regulators and with proliferative activities in PNET tissues. In addition, expression induced decrease expression of multiple cell cycle related gene (CCNA2, CCNB1, CDK1, CDK2) and inhibited cell cycle in a PNET cell line (QGP1).
These results suggested that PRA is closely associated with inhibition of cell cycle and can be a target molecule in treatment for patients with PNET.
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