| Project/Area Number |
03671172
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Hematology
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| Research Institution | Hokkaido University |
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Principal Investigator |
SAWADA Ken-ichi Hokkaido University Hospital Lecturer, 医学部・附属病院, 講師 (90226069)
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| Co-Investigator(Kenkyū-buntansha) |
佐藤 典宏 北海道大学, 医学部・附属病院, 医員
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| Project Period (FY) |
1991 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1993: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1992: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1991: ¥600,000 (Direct Cost: ¥600,000)
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| Keywords | Meylodysplastic syndrome / CD34 / Serum-free medium / Colony-stimulating factor / Granulocyte colony-stimulating factor / 骨髄異形成症侯群 / 骨髄異形成症候 / 再生不良性貧血 / 純化幹細胞 / 再生不良性質血 |
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| Research Abstract |
The presence of serum or contaminant cells may alter clonal development of haematopoietic progenitor cells in vitro. To investigate the pathogenesis of myelodysplastic syndromes (MDS), marrow progenitor cells from thirteen MDS patients were highly purified using monoclonal antibodies including CD34 and immunomagnetic microspheres. The cells positive for CD34 in the purified cells were in a range from 87 to 98 %. These purified cells were cultured in serum-free medium with individual colony stimulating factors (CSFs) to investigate whether CD34^+ cells from MDS patients have abnormal responses to individual CSFs.
Dose response experiments with the purified CD34^+ cells and recombinant human macrophage-CSF (rM-CSF), granulocyte-CSF (rG-CSF), granulocyte/macrophage-CSF (rGM-CSF), interleukin-3 (rIL-3) or erythropoietin (rEP) were performed in serum-free fibrin clots in eleven patients. Five patients showed a diminished response to rG-CSF and one patient to rEP.In the remaining six patients, the purified CD34^+ cells did not respont to a stimulation of any individual CSFs. The results indicate that the progenitor cell growth abnormalities in these disorders involve a defect in the capacity of progenitor cells to respond to stimulation with G-CSF, and present direct evidence for the manner in which myelodysplastic CD34^+ cells are impaired.
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