1997 Fiscal Year Final Research Report Summary
ABNORMALITIES IN DNA REPAIR AND GENOMIC IMPRINTING IN ORAL PRECANCEROUS LESIONS.
| Project/Area Number |
08672280
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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 |
Surgical dentistry
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
CHIBA Itsuo HOKKAIDO UNIVERSITY SCHOOL OF DENTISTRY INSTRUCTOR, 医学部, 助手 (50250460)
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| Co-Investigator(Kenkyū-buntansha) |
YASUDA Motoaki HOKKAIDO UNIVERSITY SCHOOL OF DENTISTRY INSTRUCTOR, 歯学部, 助手 (90239765)
SHINDOH Masanobu HOKKAIDO UNIVERSITY SCHOOL OF DENTISTRY ASSOCIATE PROFESSOR, 歯学部, 助教授 (20162802)
MORIUCHI Tetsuya HOKKAIDO UNIVERSITY SCHOOL OF MEDICINE PROFESSOR, 歯学部, 教授 (20174394)
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| Project Period (FY) |
1996 – 1997
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| Keywords | ORAL SCC / PRECANCEROUSLESION / BETEL QUID / P53 GENE / DNE REPAIR / GENETICINSTABILITY |
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| Research Abstract |
Oral squamous cell carcinoma (SCC) is the most common neoplasm in Sri Lanka, accounting for approximately 30% of all cancers in males. Epidemiologic evidence indicates that there is an unequivocal relationship between betel chewing oral carcinogenesis, suggesting there may be specific genetic targets of betel quid ingredients.The p53 gene has been indicated to be a tumor suppressor gene that is found in mutated from in common human cancers ; however, there are few reports about carcinogen-specificp 53 mutation. Because of this background, primary, resected specimens from 23 oral SCC_s,7 leukoplakias and 2 oral submucous fibrosis were collected from oral SCC patients in Sri Lanka and were used for the p53 mutation analysis. Exons 5 through 8 of p53 gene were examined using polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and direct sequencing. Mutations in the p53 gene were frequent (10/23,43%) in oral SCC specimens from Sri Lanka. Moreover, the mutations clustered significantly in exon 5 (7/10,70%) of the p53 gene and small deletions and inclusions other than point mutations were observed. These results indicate that 1) betel quid chewing may cause specific fenetic changes, including mutation in the p53 gene, 2) mutations in tthe p53 gene are not rare vvents in SCC patients who are betel quid chewers, which is in contrast to previous reports, 3) exon 5 of the p53 gene could be one of the specific targets for some betel quid ingredients, and 4) betel quid chewing may be one of the critical environmental factors in the development of oral SCC.
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