| Project/Area Number |
06304039
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| Research Category |
Grant-in-Aid for Co-operative Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Okayama University |
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Principal Investigator |
NAGAI Noriyuki Okayama University, School of Dentistry, Professor, 歯学部, 教授 (90085770)
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| Co-Investigator(Kenkyū-buntansha) |
INOMATA Kenichrou Toho University, School of Medicine, Professor, 医学部, 教授 (20116388)
KURASHIMA Chieri Toritu Synthetic Institute of Gerontology, Director Research Fellow, 主任研究員 (40161731)
NOMURA Shintaro Osaka University, School of Medicine, Associate Professor, 医学部, 助教授 (80159087)
TAKAGI Tohru Tokyo Medical and Dental University, School of Dentistry, Lecturer, 歯学部, 講師 (20124696)
TUTUMI Akira Osaka Medical University, Department of Examination, Professor, 検査部, 教授 (10032864)
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| Project Period (FY) |
1994 – 1995
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| Keywords | Ameloblastoma / Amelogenin / Malignant ameloblastoma / Uncogene / Antioncogene / p53 / In situ hybridization / PCNA |
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| Research Abstract |
Immunohistochemistry was adopted to localize enamel matrix protein (amelogenin) and basement membrane components in tooth germ and odontogenic tumors as to evaluate the functional differentiation of tumor cells. The immunohistochemical results indicated that amelogenin and basement membrane substance playd important roles during hard tissue formation in tooth germ. The tumor cells in ameloblastomas resemble amoblasts but majority of ameloblastomas were not so differentiated as to synthesize amelogenin protein. Ameloblastic fibromas did not synthesize amelogeinin protein at all. Immunohistochemistry was also used to evaluate the distribution pattern and positive rate of PCNA and the localization of c-myc protein, ras protein, and p53 protein. Different distribution patterns of proliferation cells were found between follicular type and plexiform type ameloblastomas by PCNA immunostaining. In addition, the proliferation ability was increased when ameloblastomas recured. PCNA positive rate
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in malignant ameloblastomas was significantly higher than that in benign ameloblastomas. In ameloblastomas the localization of c-myc protein varied with cell circle and showed relationship to cell proliferation. ras protein was localized in differentiated tumor cells showing no direct ralationship to cell proliferation. The abnormal distribution of p53 protein was found in 2 cases of malignant ameloblastomas and 2 cases of benign ameloblastomas showing higher PCNA positive rate. Furthermore, the distribution pattern of c-myc and ras protein in p53 abnormal ameloblastomas were similar to those in malignant ameloblastomas. These results indicated that the immunodetection of above-mentioned proteins varying in quantity and localization reflected differentiation, proliferation and malignance of ameloblastomas.
In addition in situ hybridization was performed to observe amelogenin mRNA signals in rat incisors and in human odontogenic tumors. The probe was made from human plexiform type ameloblastoma and labeled by Digoxigenin. Amelogenin mRNA was mainly present in columnar cells located in the periphery of the folicles. Amelogenin mRNA was commonly observed in the tumor cells of adenoid odontogenic tumors, which also showed presence of amelogenin protein. From these findings it is concluded that adenoid odontogenic tumors were better differentiated than ameloblastomas in respect to the synthesis of amelogenin protein and mRNA. Less
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