Project/Area Number |
11671864
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
病態科学系歯学(含放射線系歯学)
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Research Institution | NIIGATA UNIVERSITY |
Principal Investigator |
SUZUKI Makoto NIIGATA UNIVERSITY, Dental Hospital Lecture, 歯学部・附属病院, 講師 (50107778)
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Co-Investigator(Kenkyū-buntansha) |
IDA Hiroko NIIGATA UNIVERSITY, Faculty of Dentistry Assistant Professor, 歯学部, 助手 (60293213)
OHSHIRO Kazufumi NIIGATA UNIVERSITY, Faculty of Dentistry Assistant Professor, 歯学部, 助手
CHENG Jun NIIGATA UNIVERSITY, Faculty of Dentistry Associate Professor, 歯学部, 助教授 (40207460)
KIMURA Shin NIIGATA UNIVERSITY, Faculty of Dentistry Asssistant Professor, 歯学部, 助手 (80251825)
SAKU Takashi NIIGATA UNIVERSITY, Faculty of Dentistry Professor, 歯学部, 教授 (40145264)
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Project Period (FY) |
1999 – 2000
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Project Status |
Completed (Fiscal Year 2000)
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Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2000: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1999: ¥2,500,000 (Direct Cost: ¥2,500,000)
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Keywords | salivary gland / pleomorphic adenoma / precancerous lesion / biopsy / capsular invasion / cancer suppressor gene / p53 / PCR / 唾液腺 / 多形性腺腫 / 前癌病変 / 生検 / 被膜浸潤 / 癌抑制遺伝子 / p53 / PCR / 多形性腺腫内癌腫 / 細胞周期マーカー / PCNA |
Research Abstract |
To establish a notion of the precancerous lesion of the salivary gland, we screened surgical pathology tissue sections of salivary gland, we came to focus on pleomorphic adenomas in terms of the presence of atypical cells and capsular invasion. We studied clinicopathologically the frequency and variation of cellular atypia among tumor cells and immunohistochemically for expression status of p53 gene products as well as proliferating cell nuclear antigen(PCNA)in 101 surgical materials of pleomorphic adenomas. Histopathologically, atypical tumor cells were found in 60% of the cases examined. Their mode of distribution was classified into three groups : focal(6 cases, 6%), which could be identified as focal carcinoma, measuring less than 1 mm in diameter ; sporadic(15 cases, 15%)and singular(30 cases, 30%). These atypical cells were located mainly within sheet-like nests of tumor cells but not in chondroid or fibro-hyaline foci. Immunohistochemically, most of the atypical cells were positi
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ve for p53 gene products and PCNA.The results indicated that atypical cells with p53 protein accumulation in their nuclei could be regarded as cells in a precancerous state, and that the foci which include these atypical cells are likely to mature to focal carcinomas and then to an apparent form of carcinoma in pleomorphic adenoma. In the next place, we examined capsular invasion of pleomorphic adenomas in the same specimens used in the above experiment. Forms of capsular invasion were divided into three types : I.expansive ; II.focally infiltrative ; III.interruptive. One of the three invasion types was at least found in all of the cases examined. Type III was rarer and tended to appear in the background of type I or type II.The invasion sites with types I and II had a characteristic histology of stellate cells in myxoid stroma Hence, the myxoid stroma, which is poor in vascularity, seemed to be quite fertile in proliferation of tumor cells. However, in the invasion site with type III, there was a solid proliferation of tumor cells with tubule formation. Furthermore, vascular invasion by tumor cells was often observed. The results indicate that pleomorphic adenoma should not be regarded as a mere benign tumor but that its semi-malignant or premalignant nature should be stressed. Less
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