| Project/Area Number |
02454373
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Urology
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| Research Institution | Keio University |
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Principal Investigator |
HAYASHI Satoru (1992) Keio Univ., Sch. of Med. Dept. of Urology, Assistant, 医学部, 助手 (60180965)
畠 亮 (1990-1991) 慶應義塾大学, 医学部, 助教授 (40051586)
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| Co-Investigator(Kenkyū-buntansha) |
HATA Makoto Tokyo Dental College. Dept. of Urology, Professor, 歯学部, 教授 (40051586)
SAITO Shiro Keio Univ., Sch. of Med. Dept. of Urology, Assistant, 医学部, 助手 (80170504)
BABA Shiro Keio Univ., Sch. of Med. Dept. of Urology, Assistant Professor, 医学部, 講師 (00051889)
林 暁 慶應義塾大学, 医学部, 助手 (60180965)
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| Project Period (FY) |
1990 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥4,400,000 (Direct Cost: ¥4,400,000)
Fiscal Year 1992: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1991: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1990: ¥3,000,000 (Direct Cost: ¥3,000,000)
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| Keywords | Renal Cell Carcinoma / Chromosom / G-banding technique / Transitional Cell Carcinoma / H-ras oncogene / Point Mutation / Hーras / オンコジン / 泌尿器系腫瘍 |
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| Research Abstract |
We started this study in aiming to clarify the mechanism of genesis and proliferation of renal malignant tumors by means of molecular biology technique utilizing tissue materials surgically extirpated from the patients with renal cell carcinoma.
In the 1st year, chromosomal analysis was carried out on 8 tumors of renal cell carcinoma. There were relatively high incidence of numerical aberrations in #3 and #7 chromosoms, and a lesser incidence of constitutional aberrations, i.e. long-arm aberrations in #2 and #6 chromosoms.
In the 2nd year, DNAs were extracted from these 8 tumors and then subjected to evaluation of various oncogene expression. However, no significant abnormaility was found. On the other hand, it was successful to detect over expression of H-ras oncogene and its point mutation by means of polymerase chain reaction(PCR) method in 2 out of 50 bladder cancers (4%). In this method, the DNA segments including codon 12 were amplified by PCR, and the reaction products were examined for their susceptibility to the restriction enzyme, and by dot blot hybridization assay with oligonucleotide probes.
Point mutations were detectable in small amounts of DNAs isolated from fresh or frozen tumor tissues, urine cells and paraffin sections. These results indicated that our method was not superior as screening,but very useful in following up the readily positive cases. Particularly emphasized is feasibility of urine cells as test samples because of their non invasiveness to the patients and easy repeatability.
In the 3rd year, we made efforts to try to publicate our results.
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