| Project/Area Number |
05671690
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Surgical dentistry
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| Research Institution | NIHON UNIVERSITY |
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Principal Investigator |
KUSAMA Kaoru NIHON UNIV., SCH of DENT,LECTURER, 歯学部, 講師 (20130479)
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| Co-Investigator(Kenkyū-buntansha) |
ODA Yasuyuki NIHON UNIV., SCH of DENT,ASSISTANT, 歯学部, 助手 (60214144)
KUDO Itsuro NIHON UNIV., SCH of DENT,PROFESSOR, 歯学部, 教授 (90059147)
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| Project Period (FY) |
1993 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1995: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1994: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1993: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | oncogene / oncoprotein / gene alteration / oral cancer / squamous cell carcinoma / ras gene / c-erbB1 / c-erbB2 / ras P21 / EGFR / c-erbB-1 / c-erbB-2 / 点突然変異 / 増幅 / 口腔腫瘍 / 唾液腺腫瘍 / ras遺伝子 / ras p21 / c-erbB |
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| Research Abstract |
Expression of oncoproteins such as ras p21, EGFR and c-erbB2 protein in various kinds of oral epithelial lesions including squamous cell carcinoma (SSC) was examined by an immunohistochemical method. Weak or few reaction for c-erbB2 protein was found in the tissues of oral SSCs. On the other hand, strong reaction for ras p21 and EGFR was observed in cancer tissues and the reactivity was stronger than that in non-cancerous oral epithelial lesions. Although the presence of point mutation in codon 12 of H-ras gene in some SSC cases was suggested by Msp I digestion method, no alterations in H- and K-ras genes were identified in any cases of SSC by direct sequence and SSCP methods, Amplification of c-erbB1 was found in one third of SSC cases by Southern hybridization, which were classified into Stage I,suggesting that the alteration of c-erbB1 may be related to the early stage of oral SSC.Strong reaction for ras p21 was found in all cases of salivary gland tumor by an immunohistochemical method. In adenoid cystic carcinoma the reactivity for c-erbB2 protein was stronger than that for EGFR.Althogh the alteration of K-ras gene was suggested by TGGE in pleomorphic adenomas, no amplification of c-erbB1 and c-erbB2 was detected in adenoid cystic carcinomas by Southern hybridization. In addition to these results, enhanced expression of p53 protein and tha alteration of p53 gene were observed in one third of epithelial dysplasias and oral SSCs. This result suggests that p53 gene mutation may be involved in carcinogenesis in the oral squamous epithelium even in the early stage of the dysplasia-carcinoma sequence.
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