1999 Fiscal Year Final Research Report Summary
Analysis of biologically active substances in volved in growth regulation of leukemia cells
| Project/Area Number |
10670715
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Yamanashi Medical University |
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Principal Investigator |
SUGITA Kanji Yamanashi Medical University, Department of Pediatrics, Assistant professor, 医学部, 講師 (60138055)
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| Co-Investigator(Kenkyū-buntansha) |
手塚 徹 山梨医科大学, 医学部, 助手
INUKAI Takeshi Yamanashi Medical University, Department of Pediatrics, Assistant, 医学部, 助手 (30293450)
TZUKA Toru Yamanashi Medical University, Department of Pediatrics, Assistant
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| Project Period (FY) |
1998 – 1999
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| Keywords | leukemic cells / physiologically active substances / proliferation / apoptosis |
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| Research Abstract |
We evaluated effects of a variety of biologically active substances on growth regulation of leukemia cells. We found that proliferation of leukemic cells with Philadelphia chromosome and 11q23 translocation is stimulated by an addition of granulocyte colony-stimulating factor (G-CSF). Moreover, their proliferation was partially inhibited by exogenously added anti-G-CSF monoclonal antibody, suggesting that the GCSF/G-CSF receptor interaction is implicated in the growth regulation of these leukemia cells in a autocrine mechanism. We also showed that a specific inhibitor of tyrosine kinase having JAK-2 activity (AG490) was capable of inducing induction of B-precursor leukemia cells without effect on normal hematopoietic stem cells, suggesting that use of this drug might be useful for ex vivo purging of these leukemic cells for autologous stem cell transplantation. We also showed that erythropoietin and leptin have a moderate stimulatory activity on proliferation of B-precursor leukemia cells, whereas transforming growth factor β has a marked inhibitory activity. These results suggest that these biologically active substances are closely involved in determining destiny of leukemia cells and may be applicable for the treatment of leukemia.
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[Publications] Inukai T, Sugita K, Iijima K, Goi K, Tezuka T, Kojika S, Kagami K, Mori T, Kinoshita A, Suzuki T, Koyama T-O, Nakazawa S.: "Leukemic cells with 11q23 translocation express granulocyte colony-stimulating factor (G-CSF) receptor and their proliferation is stimulated with G-CSF."Leukemia. 12. 382-389 (1998)
Description
「研究成果報告書概要(欧文)」より
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[Publications] Sugita K, Mori T, Yokota S, Kuroki Ma, O-Koyama T, Inukai T, Iijima K, Goi K, Tezuka T, Kojika S, Shiraishi K, Nakamura M, Miyamoto N, Karakida N, Kagami K, Nakazawa S.: "The KOR-SA3544 antigen predominantly expressed on surface of Philadelphia chromosome-positve acute lymphoblastic cells is nonspecific cross-reacting antigen-50/90 (CD66c) and invariably expressed in cytoplasm of human leukemia cells."Leukemia. 13. 779-785 (1999)
Description
「研究成果報告書概要(欧文)」より
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[Publications] Nakamura M, Sugita K, Inukai T, Goi K, Iijima K, Tezuka T, Kojika S, Shiraishi K, Miyamoto N, Karakida N, Kagami K, O-Koyama T, Mori T, Nakazawa S.: "p16/MTS1/INK4A gene is frequently inactivated by hypermethylation in childhood acute lymphoblastic leukemia with 11q23 translocation."Leukemia. 13. 884-890 (1999)
Description
「研究成果報告書概要(欧文)」より
