| Project/Area Number |
09307047
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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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 | TOKYO MEDICAL AND DENTAL UNIVERSITY |
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Principal Investigator |
ENOMOTO Shoji TOKYO MEDICAL AND DENTAL UNIVERSITY,FACULTY OF DENTISTRY,PROFESSOR, 歯学部, 教授 (40013940)
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| Co-Investigator(Kenkyū-buntansha) |
HIRANO Yasumasa TOKYO MEDICAL AND DENTAL UNIVERSITY,FACULTY OF DENTISTRY,INSTRACTOR, 歯学部, 助手 (00302878)
SAKAI Eiki TOKYO MEDICAL AND DENTAL UNIVERSITY,FACULTY OF DENTISTRY,INSTRACTOR, 歯学部, 助手 (60292976)
上田 晶義 東京医科歯科大学, 歯学部, 助手 (00272609)
草間 幹夫 東京医科歯科大学, 歯学部, 講師 (60124690)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥21,100,000 (Direct Cost: ¥21,100,000)
Fiscal Year 1998: ¥6,100,000 (Direct Cost: ¥6,100,000)
Fiscal Year 1997: ¥15,000,000 (Direct Cost: ¥15,000,000)
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| Keywords | Squamous cell carcinoma (SCC) / Premalignant lesions / leukoplakia or erythroplakia / p53 tumor suppressor gene / diagnostic marker / lmmunohistochemical analysis / clinical prognosis / pathological malignancy score / survival rate / PCR法 / 塩基配列決定法 |
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| Research Abstract |
Squamous cell carcinoma (SCC) constitutes vast majority of the oral malignancy. The surgical treatment of oral SCC causes severe postoperative disfunction or, disfigurement. To minimize these problems, it is important to trea the patients immediately, based on the accurate diagnoses. It is well understood that some oral SCCs are developed from its premalignant lesions such as leukoplakia or erythroplakia, which give us hints to understand the mechanism of oral SCC carcinogenesis.
In this study, we examined the status of p53 tumor suppressor gene in these oral premalignant lesions, which we showed to be mutated in 2/3 of oral SCCs, and if the p53 alteration could be used as a diagnostic marker of the premalignant lesions expected to be transformed into SCC later. Immunohistochemical analysis showed that p53 protein was highly expressed in many cases of the oral leukoplakia which were found to be subsequently transformed into SCC, suggesting that p53 gene alteration may possibly occur prior to malignant transformation. This result indicate that p53 alteration may possibly serve as a diagnostic marker of oral. SCC premalignant lesions.
In addition, p53 gene mutation and clinical prognosis of the patient was compared to know the role of the gene in the progression of oral SCC.We could not find obvious correlation between the status of p53 and pathological malignancy score, the rate of recurrence and survival rate, suggesthig that p53 may possibly play a role rather in the initiation than prpgression of oral SCC.
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