| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1998: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1997: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1996: ¥700,000 (Direct Cost: ¥700,000)
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| Research Abstract |
Numerical aberrations of chromosome 17 was studied by fluorescence in situ hybridization (FISH) using pericentromere specific DNA probe in 27 oral squamous cell carcinoma (SCC), and its relationship with p53 and Bcl-2 protein expression was investigated. Since cells with polysomy 17 significantly increased in SCC (p=0.0005), chromosome 17 abnormality seems to be correlated with carcinogenesis of oral SCC.Chromosome 17 abnormality varied from case to case, and the degree of the abnormality did not correlate with the stage of the disease, the histological differentiation of SCC, relapse of the disease and lymph node matastasis . However, there was the correlation between polysomy 17 and p53 immunoreactivity (p=0.0228). p53 immunoreactivity showed correlation with relapse of the disease (p=0.044 1). An inverse relationship was found between p53 and Bcl-2 immunoreactivity (p=0.042 1). In conclusion, we suggest that polysomy 17 is in close relation to carcinogenesis of oral SCC, and that polysomy 17 significantly correlated with p53 overexpression. The possible mechanism of this phenomenon is assumed that polysomy 17 correlates with mutation of p53 which results in an accumulation of aberrant p53 protein, and that its activation causes an increase of p53 protein.
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