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

Chromosomal and genetic abnormalities in ependymomas detected by fluorescence in situ hybridization or microarray assay

Research Project

Project/Area Number 17591528
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Cerebral neurosurgery
Research InstitutionSaitama Medical University

Principal Investigator

ADACHI Jun-Ichi  Saitama Medical University, Neurosurgery, Instructor (70291143)

Co-Investigator(Kenkyū-buntansha) NISHIKAWA Ryo  Saitama Medical School, Neurosurgery, Professor (90237678)
MATSUTANI Masao  Saitama Medical School, Neurosurgery, Professor (90010454)
Project Period (FY) 2005 – 2006
Project Status Completed (Fiscal Year 2006)
Budget Amount *help
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2006: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2005: ¥2,300,000 (Direct Cost: ¥2,300,000)
KeywordsEpendymoma / DNA chip / Genetic abnormality / FISH / 脳腫瘍
Research Abstract

Ependymomas account for approximately 3-5% of central nervous system (CNS) tumors. These entities have not yet been subjected to systematic chromosomal and genetic studies. We conducted immunohistochemistry, fluorescence in situ hybridization (FISH) analysis and microarray assay on 37 ependymomas and examined the correlation of chromosomal abnormalities with clinicopathological findings. Paraffin-embedded surgical specimens for 22 intracranial and 15 spinal ependymoma cases were obtained from Saitama Medical School Hospital and its collaborating hospitals (Tokyo Univ., Hiroshima Univ., Hokkaido Univ., Kyorin Univ., Dokkyo University School of Medicine, Otsu Municipal Hospital and Showa General Hospital) in Japan. Human bacterial artificial chromosome (BAC) clones specific to each chromosomal locus were used as FISH probes. BAG DNA was labeled using the Nick Translation method. Eleven (50%) of 22 grade II ependymomas had increased numbers of chromosome 5, regardless of localization of the tumors. Deletions at chromosome 22q12.2 (within the NF2 gene) were found in 3 (13.6%) of 22 intracranial and 8 (53.3%) of 15 spinal ependymomas. Deletions at chromosome 17p13.3 were detected in none of 23 grade II ependymomas and 6 (40%) of 15 anaplastic ependymomas. The incidence of chromosome 17p13.3 loss in anaplastic ependymomas was significantly higher than that in grade II ependymomas (p < 0.01). These results suggest that chromosome 5 aberrations and alteration of the NF2 gene are involved in a subset of grade II ependymomas and spinal ependymomas, respectively. It is possible that chromosome 17p13.3 loss occurs late in the progression of ependymomas and/or causes phenotypic changes of ependymoma cells into more aggressive ones.

Report

(3 results)
  • 2006 Annual Research Report   Final Research Report Summary
  • 2005 Annual Research Report
  • Research Products

    (2 results)

All 2007

All Presentation (2 results)

  • [Presentation] Chromosomal and genetic abnormality in ependymoma detected by fluorescence in situ hybri dization2007

    • Author(s)
      中島 弘之, 安達 淳一, ら
    • Organizer
      5th.Meeting of the Asian Society for Neuro-Oncology
    • Place of Presentation
      イスタンブール,トルコ
    • Year and Date
      2007-11-02
    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Presentation] Chromosomal and genetic abnormality in ependymoma detected by fluorescence in situ hybridization.2007

    • Author(s)
      Nakajima H, Adachi J, Hirose T, Matsutani M and Nishikawa R
    • Organizer
      5th. Meeting of the Asian Society for Neuro-oncology
    • Place of Presentation
      Istanbul, Turkey
    • Year and Date
      2007-11-02
    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2006 Final Research Report Summary

URL: 

Published: 2005-04-01   Modified: 2016-04-21  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi