1997 Fiscal Year Final Research Report Summary
Esophageal Carcinogenesis in the High-risk Area-HPV infection and genetic abnormality, expression of HLA antigen-
Project/Area Number |
08042006
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Research Category |
Grant-in-Aid for international Scientific Research
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Allocation Type | Single-year Grants |
Section | Special Cancer Research |
Research Field |
Molecular biology
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Research Institution | KYUSHU UNIVERSITY |
Principal Investigator |
SUGIMACHI Keizo Faculty of Medicine, Kyushu University, Department of Surgery II,Professor, 医学部, 教授 (00038762)
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Co-Investigator(Kenkyū-buntansha) |
MORITA Masaru Faculty of Medicine, Kyushu University, Department of Surgery II,Assistant, 医学部, 助手 (30294937)
KITAMURA Kaoru Faculty of Medicine, Kyushu University, Department of Surgery II,Assistant, 医学部, 助手 (70234276)
KUWANO Hiroyuki Faculty of Medicine, Kyushu University, Department of Surgery II,Assistant Profe, 医学部, 助教授 (90186560)
RU Gang Zhang Department of Thoracic Surgery, Cancer Hospital, Chinese Academy of Medical Sien, 教授
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Project Period (FY) |
1996 – 1997
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Keywords | Esophageal Cancer / Precancerous Lesion / p53 / Human Papillomavirus / HLA-DR / Smoking / Drinking / Family History |
Research Abstract |
To elucidate the association of Human Papillomavirus (HPV) with carcinogenesis of the esophagus, esophageal squamous cell .carcinomas in Japan and China were examined for the presence of HPV DNA by polymerase chane reaction (PCR). PCR showed that 4.3%(1/23) contained HPV in Japannese cases and 22.2%(28/126) in Chinese cases(p<0.05) excluded high risk group of esophageal carcinoma. These results suggested tat the HPV DNA might play a role in carcinogenesis of the esophagus at least in Chinese cases. The number of heavy drinkers and smokers were 31.8% and 30.0% in Japanese cases, and 7.9% and 5.3% in Chinese cases, respectively (p<0.0001). In Japanese cases, frequency of the p53 protein accumulations in cases with heavy smokers was higher than that with light smokers (p<0.0l). The similar result was observed in the comparison between the cases with heavy drinkers and light drinkers (p<0.01). Furthermore, the p53 protein accumulations were found in 9 of 25 (36.0%) in patients having both histories of light smoking and light drinking, whereas in 14 of 15 (93.3%) in patients having both histories of heavy smoking and heavy drinking (p<c0.05). We conclude that cigarette smoking and alcohol drinking caused a high frequency of the p53 protein accumulation in patients with esophageal squamous cell carcinoma and it is considered to be a main pathway of esophageal carcinogenesis in Japan.
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