2001 Fiscal Year Final Research Report Summary
Analysis of carcinogenic process of oral leukoplakias and establishment of their treatment
| Project/Area Number |
11671971
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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 Univ., Grad. School of Dental Medicine, 医学部・附属病院, 講師 (50250460)
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| Co-Investigator(Kenkyū-buntansha) |
KOBAYASHI Ichizo Hokkaido Univ., Grad. School of Dental Medicine, 大学院・歯学研究科, 講師 (70170305)
SHINDOH Masanobu Hokkaido Univ., Grad. School of Dental Medicine, 大学院・歯学研究科, 助教授 (20162802)
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| Project Period (FY) |
1999 – 2001
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| Keywords | Leukoplakia / p53 gene / premalignant lesions / oral cancer / carcinogens |
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| Research Abstract |
Leukoplakia and oral submucous fibrosis (OSMF), which is affected whole oral mucosa, are thought to be premalignant lesion/condition. Oral lichen planus (OLP) is categorized as a 'probable precancerous condition', however, the etiology is still unknown. Small scale analyzes have been done, however, it is difficult to analyze the nature of the mutations because of low ftequency. We analyzed 115 leukoplakias, 22 oral lichen planus and 32 oral submucous fibrosis for detecting mutations in the p53 gene using yeast functional assay (YFA). Thirteen mutations in 169 cases (7.7 %), including 8 of leukoplakia, 3 of OLP and 2 of OSMF, were detected and no correlation between the incidence of mutations and the severity of dysplasia. These data suggest that 1) YFA is a sensitive method for detecting mutations in oral premalignancies ; 2) p53 mutation could be independent on severity of dysplastic changes ; and 3) these molecular events could be an important evidence for field cancerization
We investigated the relationship between inter-individual difference in CYP2A6 genotype and susceptibility to oral cancer. A total of 286 subjects showing oral malignant or premalignant lesions and 135 control subjects with no lesions were analyzed. The frequency of homozygotes for CYP2A6^*4Cmutation, a gene deletion type of polymorphism, was significantly lower in the case subjects than the controls. The odds ratio (OR) of the group homozygous for the deletion was significantly lower and calculated to be 0.14 (95 % CI ; 0.03-0.72). In the allelic base analysis, there was also a significant decrease in the OR of the deletion allele. Our data suggest that deficient CYP2A6 activity due to genetic polymorphism reduces oral cancer risk.
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