Molecular/cellular biological analysis of pathogenesis and spontaneous remission mechanism in Down syndrome transient myeloproliferative disorder
Project/Area Number |
23591552
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Pediatrics
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Research Institution | Tokyo Dental College |
Principal Investigator |
MIYAUCHI Jun 東京歯科大学, 歯学部, 教授 (20146707)
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Co-Investigator(Kenkyū-buntansha) |
KAWAGUCHI Hiroyuki 防衛医科大学校, 小児科, 講師 (00313130)
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Project Period (FY) |
2011 – 2013
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Project Status |
Completed (Fiscal Year 2013)
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Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | 一過性骨髄増殖症 / ダウン症候群 / 造血微小環境 / 造血因子 / 胎児造血 / 胎児肝間質細胞 / 自然治癒 / GM-CSF / 上皮間葉転換 / 間葉系幹細胞 / 一過性白血病 |
Research Abstract |
In neonates with Down syndrome, hematological abnormalities similar to acute myeloid leukemia may be seen but usually spontaneously disappear. This disorder, called transient myeloproliferative disorder (TMD), is thought to be a unique myeloid neoplasm arising in the fetal liver. The mechanism of its spontaneous remission is unclear. In this study, using cell culture techniques, we demonstrated that stromal cells constituting microenvironment of the fetal liver support the growth of TMD blasts and that one of the hematopoietic growth factors, granulocyte-macrophage colony-stimulating factor (GM-CSF), produced by the stromal cells play an important role. These results indicate that fetal hematopoietic microenvironment is involved in the onset, progression and spontaneous remission of TMD.
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Report
(4 results)
Research Products
(75 results)
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[Journal Article] Targeted inactivation of nuclear interaction partner of ALK (NIPA) disrupts meiotic prophase2013
Author(s)
Illert AL, Kawaguchi H, Antinozzi C, Bassermann F, de Fend LQ, von Klitzing C, Hiwatari M, Peschel C, de Rooij DG, Morris SW, Barchi M, Duyster J
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Journal Title
Development
Volume: 139
Issue: 14
Pages: 2523-2534
DOI
Related Report
Peer Reviewed
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[Journal Article] Somatic mosaicism for oncogenic NRAS mutations in juvenile myelomonocytic leukemia2012
Author(s)
Doisaki S, Muramatsu H, Shimada A, Takahashi Y, Mori-Ezaki M, Sato M, Kawaguchi H, Kinoshita A, Sotomatsu M, Hayashi Y, Furukawa-Hibi Y, Yamada K, Hoshino H, Kiyoi H, Yoshida N, Sakaguchi H, Narita A, Wang X, Ismael O, Xu Y, Nishio N, Tanaka M, Hama A, Koike K, Kojima S
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Journal Title
Blood
Volume: 120
Issue: 7
Pages: 1485-1488
DOI
Related Report
Peer Reviewed
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[Journal Article] Targeted inactivation of nuclear interaction partner of ALK (NIPA) disrupts meiotic prophase.2012
Author(s)
Illert AL, Kawaguchi H, Antinozzi C, Bassermann F, Quintanilla de Fend F, von Klitzing C, Hiwatari M, Peschel C, de Rooij DG, Barchi M, Morris SW, Duyster J
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Journal Title
Development
Volume: in press
Related Report
Peer Reviewed
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[Presentation] A case of splenectomy to stage IV splenic DLBCL with PET-positive residual disease before auto PBSCT2011
Author(s)
Okada S, Watanabe T, Hirose T, Miura K, Katoh M, Yamafuji K, Akatsuka S, Miyauchi J, Mori S, Kikuchi M, Kanda Y
Organizer
第73回日本血液学会学術集会
Place of Presentation
名古屋市
Related Report
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[Presentation] A case of splenectomy to stage IV splenic DLBCL with PET-positive residual disease before auto PBSCT2011
Author(s)
Okada S, Watanabe T, Hirose T, Miura K, Katoh M, Yamafuji K, Akatsuka S, Miyauchi J, Mori S, Kikuchi M, Kanda Y
Organizer
第73回日本血液学会学術集会
Place of Presentation
名古屋国際会議場(名古屋市)
Related Report
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[Presentation] Loss of NIPA leads to defects in the repair of DNA double strand breaks in mice
Author(s)
Illert A, Antinozzi C, Kawaguchi H, Kulinski M, Klitzing C, Peschel C, de Rooji D, Morris SW, Barchi M, Duyster J
Organizer
55th annual meeting of American society of Hematology
Place of Presentation
New Orleans, LA, USA
Related Report
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