| Project/Area Number |
14571730
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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 |
Morphological basic dentistry
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| Research Institution | Gifu University |
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Principal Investigator |
TOIDA Makoto Gifu University, School of Medicine, Associate Professor, 医学部, 助教授 (90313890)
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| Co-Investigator(Kenkyū-buntansha) |
FUJITSUKA Hideki Gifu University, Hospital, Lecturer, 医学部附属病院, 助手 (90262766)
YAMASHITA Tomomi Gifu University, Hospital, Senior Lecturer, 医学部附属病院, 講師 (80345793)
MAKITA Hiroki Gifu University, Hospital, Lecturer, 医学部附属病院, 助手 (50345790)
SHIBATA Toshiyuki Gifu University, School of Medicine, Professor, 医学部, 教授 (50226172)
KATO Yukihiro Gifu University, School of Medicine, Lecturer, 医学部, 助手 (30293567)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 2003: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2002: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | odontogenic tumor / ameloblastoma / comparative genomic hybridization / genetic alteration / chromosomal alteration / proliferative activity / comparative genomic hybridization法 / 遣伝子異常 |
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| Research Abstract |
Comparative genomic hybridization (CGH) is a molecular cytology technique that allows rapid detection of chromosome copy number alterations through the entire tumor genome in a single hybridization reaction. However, there have been a few CGH repolls of chromosomal alterations in odontogenic tumors. In order to define and map chromosomal copy number alterations in ameloblastomas, which is one of the most popular odontogenic tumors, of the jaw bones, CGH and fluorescence in situ hybridization (FISH) techniques were applied for 10 tumors of this type. Only in 1 out of the 10 cases, chromosomal alterations were detected by CGH ; those included gain at 1q and losses at 1pter, 10q, and 22q. In this case, FISH analysis using chromosome 1 centromeric probe revealed significant increase of trisomic cells, which accounted for 41.2% of all tumor cells examined. Also in another case, significant increase of trisomic cells (15.4%) were detected. Moreover, in 5 out of the rest 8 cases, 10-33% of monosomic cells were observed. Furthermore, in the case in which alterations were detected by CGH. 21.4% of monosonic cells and 22.0% of trisomic cells were detected by FISH analysis using specific probe for 10q26 region. These FISH results, which are well agreed with the CGH results, indicate that the alterations at these chromosomal regions may be involved in pathogenesis of ameloblastomas. Further studies using additional various kinds of probes in much more cases are necessary. This study has been supported by Dr. M. Balazs and Prof. R. Adany, University of Debrecen, Hungary. and it is in progress.
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