1988 Fiscal Year Final Research Report Summary
Studies on the mechanism by which leukemic blast progenitors grow indefinitely.
| Project/Area Number |
62570538
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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 | Tokyo Medical and Dental University |
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Principal Investigator |
NARA Nobuo Tokyo Medical and DEntal University, Faculty of Medicine, 医学部, 助手 (00142258)
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| Co-Investigator(Kenkyū-buntansha) |
MUROHASHI Ikuo Tokyo Medical and Dental University, Faculty of Medicine, 医学部, 助手 (90182146)
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| Project Period (FY) |
1987 – 1988
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| Keywords | Acute myeloblastic leukemia / Leukemic blast progenitor / Self-renewal / Growth factor / Receptor / サイトカイン |
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| Research Abstract |
The purpose of this study is to analyse the mechanism by which leukemic cells grow indefinitely in acute myeloblastic leukemia (AML) patients. AML is a clonal hemopathy with the progressive accumulation of leukemic blasts and the decreased normal hemopoiesis. The accumulation of blasts is maintained by only a small subpopulation, leukemic blast progenitors. Leukemic blast progenitors may renew themselves and/or undergo terminal divisions with limited differentiation. The growth and differentiation of blast progenitors were studied in methylcellulose and suspension cultures in the present study. The results show that normal granulopoietic growth factor such as G-CSF, GM-CSF, M-CSF, and IL-3 stimulate the growth of blast progenitors. The receptors for GM-CSF and IL-1 were noted on blasts.
In term of therapy for AML, the self-remewal activity of blast progenitors should be eliminated completely because the self-renewal capacity is highly correlated with clinical outcome. In the present study we confirmed that cytosine arabinoside, interferon, tumor necrosis factor and transforming growth factor were effective against the self-renewal of blast progenitors.
In the future work, we would like to determine the mechanism of leukemic cells growth more precisely and develope more efficient therapy for AML.
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