Exploitation of MICA gene polymorphism for development of personalized medicine in oral cancer patients
| Project/Area Number |
16592002
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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 |
Surgical dentistry
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
TANI Ryouji Hiroshima University, Hospital, Assistant, 病院, 助手 (10291486)
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| 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)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| 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)
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| Keywords | NK 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 |
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| 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.
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Report
(3 results)
Research Products
(4 results)
