• Search Research Projects
  • Search Researchers
  • How to Use
  1. Back to previous page

Microarray Analyses of Molecular Pathways Associated with Pathogenesis

Research Project

Project/Area Number 12204012
Research Category

Grant-in-Aid for Scientific Research on Priority Areas

Allocation TypeSingle-year Grants
Review Section Biological Sciences
Research InstitutionNational Cancer Center Research Institute

Principal Investigator

ICHIKAWA Hitoshi  National Cancer Center Research Institute, Cancer Transcriptome Project, Project Leader, 腫瘍発現解析プロジェクト, プロジェクトリーダー (30201924)

Co-Investigator(Kenkyū-buntansha) 水島 洋  国立がんセンター, 研究所・がん情報研究部, 室長 (50219630)
Project Period (FY) 2000 – 2004
Project Status Completed (Fiscal Year 2004)
Budget Amount *help
¥35,100,000 (Direct Cost: ¥35,100,000)
Fiscal Year 2004: ¥7,500,000 (Direct Cost: ¥7,500,000)
Fiscal Year 2003: ¥8,800,000 (Direct Cost: ¥8,800,000)
Fiscal Year 2002: ¥8,800,000 (Direct Cost: ¥8,800,000)
Fiscal Year 2001: ¥10,000,000 (Direct Cost: ¥10,000,000)
KeywordsDNA microarray / gene expression profiling / transcription network / neutrophilic differentiation / molecular pathway / acute mveloid leukemia / 遺伝子 / ゲノム / 発現制御 / 発生・分化 / 遺伝子発現制御 / DNAチップ / 白血病 / G-CSFシグナル伝達 / 遺伝子発現プロファイリング / t(8;21)転座 / AML1-MTG8
Research Abstract

The main object of this work is to develop bases and tools to investigate molecular pathways associated with pathogenesis using gene expression profiles of clinical samples. To achieve this, we selected acute myeloid leukemia as a major target, and carried out following analyses.
1. Analysis of gene expression aberration induced by leukemic fusion transcription factors: We analyzed alterations in gene expression caused by ectopic expression of AML1-MTG8, and revealed that AML1-MTG8 induces partial differentiation into promyelocytes but inhibits terminal differentiation into mature granulocytes.
2. Analysis of gene expression alteration during neutrophilic differentiation: As a basis to investigate the mechanism to cause differentiation block in AML, we analyzed gene expression alteration during neutrophilic differentiation of a mouse myeloid cell line L-GM, which was induced by G-CSF stimulation or overexpression of a transcription factor C/EBPα, C/EBPε or PU.l. This analysis revealed th … More e existence of two distinguishable gene regulation pathways to proceed the differentiation.
3. Analysis of gene expression of AML clinical samples: We analyzed gene expression of 61 clinical samples obtained from pediatric AML patients. This analysis revealed that AML has gene expression patterns specific to the chromosomal translocations such as t(8;21) and inv(16), and identified a gene expression signature that are associated with prognosis of pediatric AML.
4. Development of a pathway analysis tool: We developed a tool to estimate the activation status of the molecular pathways by comparing the expression of the pathway-specific genes that were identified in "Analysis 2". This enabled us to predict genetic aberrations to cause differentiation block in AML.
5. Analysis of genes associated with oncogenic transformation: As a basis to investigate malignant tumors other than leukemia, we analyzed gene expression alteration induced by Src transformation, and identified genes involved in anchorage-independent growth and cell motility. Less

Report

(6 results)
  • 2004 Annual Research Report   Final Research Report Summary
  • 2003 Annual Research Report
  • 2002 Annual Research Report
  • 2001 Annual Research Report
  • 2000 Annual Research Report
  • Research Products

    (20 results)

All 2006 2005 2004 2003 2002 2001 Other

All Journal Article (14 results) Publications (6 results)

  • [Journal Article] Src utilizes Cas to suppress Fhl1 in order to promote nonanchoredgrowth and migration of tumor cells.2006

    • Author(s)
      Y.Shen et al.
    • Journal Title

      Cancer Res. 66

      Pages: 1543-1552

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Cas to suppress Fh11 in order to promote nonanchoredgrowth and migration of tumor cells.2006

    • Author(s)
      Y.Shen et al.
    • Journal Title

      Cancer Res. 66

      Pages: 1543-11552

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] The oncogenic TLS-ERG fusion protein exerts different effects in hematopoietic cells and fibroblasts.2005

    • Author(s)
      J.Zou et al.
    • Journal Title

      Mol. Cell. Biol. 25

      Pages: 6235-6246

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] The oncogenic TLS-ERG fusion protein exerts different effects in hematopoietic cells and fibroblasts.2005

    • Author(s)
      J.Zou et al.
    • Journal Title

      Mol Cell. Biol 25

      Pages: 6235-6246

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Normal cells control the growth of neighboring transformed cells independent of gap junctional communication and Src activity2004

    • Author(s)
      D.B.Alexander et al.
    • Journal Title

      Cancer Res. 64

      Pages: 1347-1358

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Normal cells control the growth of neighboring transformed cells independent of gap junctional communication and Src activity.2004

    • Author(s)
      D.B.Alexander et al.
    • Journal Title

      Cancer Res. 64

      Pages: 1347-1358

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Impaired IgG production in mice deficient for heat shock transcription factor 1.2004

    • Author(s)
      S.Inoue, et al.
    • Journal Title

      J.Biol.Chem. 279

      Pages: 38701-38709

    • Related Report
      2004 Annual Research Report
  • [Journal Article] Normal cells control the growth of neighboring transformed cells independent of gap junctional communication and Src activity.2004

    • Author(s)
      D.B.Alexander, et al.
    • Journal Title

      Cancer Res. 64

      Pages: 1347-1358

    • Related Report
      2004 Annual Research Report
  • [Journal Article] Nemo-like kinase suppresses a wide range of transcription factors, including nuclear factor-κB.2004

    • Author(s)
      J.Yasuda, et al.
    • Journal Title

      Cancer Sci. 95

      Pages: 52-57

    • Related Report
      2004 Annual Research Report
  • [Journal Article] Identification of a gene expression signature associated with pediatric AML prognosis2003

    • Author(s)
      T.Yagi et al.
    • Journal Title

      Blood 102

      Pages: 1849-1856

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Identification of a gene expression signature associated with pediatric AML prognosis.2003

    • Author(s)
      T.Yagi et al.
    • Journal Title

      Blood 102

      Pages: 1849-1856

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Potential involvement of the AML1-MTG8 fusion protein in the granulocytic maturation characteristic of the t(8;21) acute myelogenous leukemia revealed by microarray analysis2002

    • Author(s)
      H.Shimada et al.
    • Journal Title

      Leukemia 16

      Pages: 874-885

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Potential involvement of the AML1-MTG8 fusion protein in the granulocytic maturation characteristic of the t(8;21) acute myelogenous leukemia revealed by microarray analysis.2002

    • Author(s)
      H.Shimada et al.
    • Journal Title

      Leukemia 16

      Pages: 874-885

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Global effects of anchorage on gene expression during mammary carcinoma cell growth reveal role of tumor necrosis factor-related apoptosis-inducing ligand in anoikis.2001

    • Author(s)
      G.S.Goldberg et al.
    • Journal Title

      Cancer Res. 61

      Pages: 1334-1337

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Publications] T.Yagi, et al.: "Identification of a gene expression signature associated with pediatric AML prognosis."Blood. 102. 1849-1856 (2003)

    • Related Report
      2003 Annual Research Report
  • [Publications] H.Shimada, et al.: "Potential involvement of the AML1-MTG8 fusion protein in the granulocytic maturation characteristic of the t(8;21) acute myelogenous leukemia revealed by microarray analysis"Leukemia. 16. 874-885 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] H.Shimada: "Potential involvement of the AML1-MTG8 fusion protein in the granulocytic maturation characteristic of the t(8 ; 21) acute myelogenous leukemia revealed by microarray analysis"Leukemia. (in press).

    • Related Report
      2001 Annual Research Report
  • [Publications] G.S.Goldberg: "Global effects of anchorage on gene expression during mamnary carcinoma cell growth reveal role of tumor necrosis factor-related apoptosis-inducing ligand in anoikis"Cancer Research. 61. 1334-1337 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] H.Shimada: "Analysis of genes under the downstream regulation of the t(8;21) fusion protein AML1-MTG8 : overexpression of the TIS11b (ERF-1, cMG1) gene induces myeloid cell proliferation in response to G-CSF."Blood. 96. 655-663 (2000)

    • Related Report
      2000 Annual Research Report
  • [Publications] S.Kobayashi: "Mouse Peg9/Dlk1 and human PEG9/DLK1 are paterrally expressed imprinted genes closely located to the maternally expressed imprinted genes : mouse Meg3/Gt12 and human MEG3."Genes Cells. 5. 1029-1037 (2000)

    • Related Report
      2000 Annual Research Report

URL: 

Published: 2001-04-01   Modified: 2018-03-28  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi