| Project/Area Number |
07671355
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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 |
Digestive surgery
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| Research Institution | Tohoku University |
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Principal Investigator |
SHINEHA Ryuzaburo (1996) Tohoku University The Second Dept.of Surgery Lecturer, 医学部, 講師 (20192106)
片山 正文 (1995) 東北大学, 医学部・付属病院, 助手 (00177411)
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| Co-Investigator(Kenkyū-buntansha) |
MIYAZAKI Shukichi Tohoku University The Second Dept.of Surgery, Research Associate, 医学部・附属病院, 助手 (50282075)
AKAISHI Takashi Tohoku University The Second Dept.of Surgery, Lecturer, 医学部・附属病院, 講師 (60191847)
NISHIHIRA Tetsuro Tohoku University The Second Dept.of Surgery, Associate Professor, 医学部, 助教授 (50101142)
標葉 隆三郎 東北大学, 医学部, 講師 (20192106)
高野 亮 東北大学, 医学部・付属病院, 助手 (30271935)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1996: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1995: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | allelotype of the esophageal carcinoma / esophageal carcinogenesis / p16 mutation in esophageal carcinoma / accumulation of genetic alterations. / 食道癌 / 微小リンパ節転移 / RCR-SSCP |
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| Research Abstract |
Allelotype of the esophageal carcinoma was examined in order to clarify candidate loci involved in carcinogenesis and/or progression of squamous cell carcinoma of the esophagus, and frequent deletions on several loci were observed. Comparison of the loci frequently deleted with clinicopathological data revealed correlation between 17q deletion and female cases, and correlation between 19q deletion and lymphnode metastasis. Deletion-mapping study on 17q showed the region commonly deleted was 17q21, where genetic linkage analysis revealed the BRCA1 locus. Further, LOH in epithelial dysplasia and early cancer of the esophagus was examined. Four loci showed frequent LOH in early carcinoma ; 3p21.3,9p22,9q31, and 17p13.Further, chromosomal bands on 3p21.3 and 9q31 were deleted even in low-grade dysplasia, although 9p22 and 17p13 were not deleted in any case in low-grade group. The p16 gene, isolated from candidate locus on 9p22, was mutated in some cases of the esophageal carcinoma. These results suggest that accumulation of genetic alterations may play an important role in the genesis and/or progression of squamous cell carcinoma of the esophagus.
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