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The significant role for the loss of CD27-expression in myelomagenesis

Research Project

Project/Area Number 14570982
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Hematology
Research InstitutionHIROSHIMA UNIVERSITY

Principal Investigator

SAKAI Akira  Hiroshima University, Medical and Dental Hospital, Assistant Professor, 医学部・歯学部附属病院, 講師 (70284221)

Co-Investigator(Kenkyū-buntansha) TANAKA Hideo  Hiroshima University, Research Institute for Radiation Biology and Medicine, Associate Professor, 原爆放射線医科学研究所, 助教授 (50243613)
Project Period (FY) 2002 – 2003
Project Status Completed (Fiscal Year 2003)
Budget Amount *help
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2002: ¥2,200,000 (Direct Cost: ¥2,200,000)
KeywordsCD27-CD70 interaction / Siva / apoptosis / multiple myeloma / CD27-CD70結合 / アポトーシス
Research Abstract

CD27 is a marker of memory B cells, and its interaction with its ligand, CD70, is very important for the differentiation into plasma cells. Although CD27 is detected on normal plasma cells, the expression of CD27 is significantly reduced with the progression of multiple myeloma (MM) including monoclonal gammopathy of undetermined significance (MGUS). CD27^+ myeloma cells are thought to represent on early phase of myeloma, since CD27^+ plasma cells from patients with MM were found to be composed of normal plasma cells (CD 19^+/CD38^<++>) and myeloma cells (CD 19^-/CD38^<++>), and monoclonality was detected in the CD27^+/CD38^<++> fraction. Given that the lack of CD27 on plasma cells is related to myelomagenesis and that the proapoptotic protein Siva is thought to bind to the cytoplasmic tail of CD27, we analyzed alterations of cell growth and genes caused by co-culturing CD27-transfected myeloma cell lines (U266, KMS-5) with CD70-transfected NIH3T3 cells. CD27-CD70 interaction could not induce apoptosis in either type of myeloma transfectant, and binding between Siva and CD2? was not detected. cDNA microarray (Human Apoptosis CHIP) analysis showed significant up-regulation of expression of the ectodermal neural cortex 1 (ENC 1) gene by CD27-CD70 interaction compared with CD27 transfection alone. These findings show that the relationship between the loss of CD27 and oncogenesis of plasma cells is not simple. It remains unclear whether the lack of CD27 leads to evasion of apoptosis

Report

(3 results)
  • 2003 Annual Research Report   Final Research Report Summary
  • 2002 Annual Research Report
  • Research Products

    (7 results)

All Other

All Publications (7 results)

  • [Publications] Katayama, Y.: "A possible role for the loss of CD27-CD70 interaction in myelomagenesis."Br.J.Haematol.. 120(2). 223-234 (2003)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] 沖川佳子: "骨髄腫細胞とCD27抗原"血液・腫瘍科. 3. 262-267 (2004)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Yuta Katayama: "A possible role for the loss of CD27-CD70 interaction in myelomagenesis"Br J Haematology. 120. 223-234 (2003)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Yoshiko Okikawa: "CD27 expression on myeloma cells"Hematology and Oncology. 148. 262-267 (2004)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Katayama, Y.: "A possible role for the loss of CD27-CD70 interaction in myelomagenesis"Br.J.Haematol.. 120(2). 223-234 (2003)

    • Related Report
      2003 Annual Research Report
  • [Publications] 沖川佳子: "骨髄腫細胞とCD27抗原"血液・腫瘍科. (in press). (2004)

    • Related Report
      2003 Annual Research Report
  • [Publications] Yuta Katayama: "A possible role for the loss of CD27-CD70 interaction in myelomagenesis"British Journal of Haematology. 120. 223-234 (2003)

    • Related Report
      2002 Annual Research Report

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Published: 2002-04-01   Modified: 2016-04-21  

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