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Exploitation of MICA gene polymorphism for development of personalized medicine in oral cancer patients

Research Project

Project/Area Number 16592002
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Surgical dentistry
Research InstitutionHIROSHIMA UNIVERSITY

Principal Investigator

TANI Ryouji  Hiroshima University, Hospital, Assistant, 病院, 助手 (10291486)

Co-Investigator(Kenkyū-buntansha) OKAMOTO Tetsuji  Hiroshima University, Graduate School of Biomedical Sciences, Professor, 大学院・医歯学総合研究科, 教授 (00169153)
TORATANI Shigeaki  Hiroshima University, Hospital, Assistant Professor, 病院・講師 (90172220)
Project Period (FY) 2004 – 2005
Project Status Completed (Fiscal Year 2005)
Budget Amount *help
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2004: ¥2,500,000 (Direct Cost: ¥2,500,000)
KeywordsNK cells / MICA gene polymorphism / oral cancer / disease susceptibility / soluble MICA / personalized medicine / NK activities / molecular target antigen / MICA遺伝子 / 免疫療法 / 遺伝子多型
Research Abstract

The MHC class | chain-related molecule A (MICA) is the ligand of NKG2D, which is activation receptor on most NK cells and antigen-specific effector T cells. These molecules are absent from most cells but can be induced by stress, infection, cell transformation and are frequently expressed in epithelial tumors. The MICA gene has a triplet repeat (GCT) polymorphism in the transmembrane domain, and relevance with the disease susceptibility of Type | -DM. To evaluate the possible association of MICA gene polymorphism with the risk for oral squamous cell carcinoma(OSCC), we analysed MICA polymorphism in cases with OSCC by direct sequencing and fragment analysis.
Five distinct MICA alleles A4,A5,A6,A9,and A5.1 were studied. MICA 5.1 variant gene contains a fournucleotide insertion that causes a stop codon in the transmembrane region. In addition, as an sMICA has been considered to cause the down regulation of NKG2D resulted in suppression of NK cells and antigen-specific effector Tcells, we have examined the concentration of soluble MICA(sMICA) in the serum of OSCC patients by ELISA assay.
As the result, we have found that the phenotype frequency of allele 5.1 of MICA and the sMICA levels in subjects with OSCC were significantly higher than those in controls.
These results suggested that susceptibility to OSCC is linked to the MICA microsatellite and A5.1 allele might confer the risk of OSCC.

Report

(3 results)
  • 2005 Annual Research Report   Final Research Report Summary
  • 2004 Annual Research Report
  • Research Products

    (4 results)

All 2004

All Journal Article (4 results)

  • [Journal Article] Cell therapy for head and neck cancer with lymphokine-activated killer cells and Vitamin A.2004

    • Author(s)
      Tani, R
    • Journal Title

      Asian journal of Oral and Maxillofacial Surgery 16

      Pages: 176-176

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Analysis of MICA gene polymorphism in oral cancer.2004

    • Author(s)
      Ikeda, J
    • Journal Title

      Asian journal of Oral and Maxillofacial Surgery 16

      Pages: 169-169

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Cell therapy for head and neck cancer with lymphokine-activated killer cells and Vitamin A2004

    • Author(s)
      Tani, R
    • Journal Title

      Asian journal of Oral and Maxillofacial Surgery 16

      Pages: 176-176

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Analysis of MICA gene polymorphism in oral cancer2004

    • Author(s)
      Ikeda, J.
    • Journal Title

      Asian journal of Oral and Maxillofacial Surgery 16

      Pages: 169-169

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2005 Final Research Report Summary

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Published: 2004-04-01   Modified: 2016-04-21  

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