2001 Fiscal Year Final Research Report Summary
Genetic analysis of multiple sproradic renal call carcinoma
| Project/Area Number |
12671555
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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 |
Urology
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| Research Institution | Keio University |
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Principal Investigator |
OYA Mototsugu Keio University, School of Medicine, Assistant Professor, 医学部, 専任講師 (00213885)
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| Co-Investigator(Kenkyū-buntansha) |
OHIGASHI Takashi Keio University, School of Medicine, Assistant Professor, 医学部, 専任講師 (80185371)
NAKASHIMA Jun Keio University, School of Medicine, Assistant Professor, 医学部, 専任講師 (10167546)
MARUMO Ken Keio University, School of Medicine, Associate Professor, 医学部, 助教授 (80138130)
MURAI Masaru Keio University, School of Medicine, Professor, 医学部, 教授 (90101956)
HORIGUCHI Yutaka Keio University, School of Medicine, Instructor, 医学部, 助手 (60229234)
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| Project Period (FY) |
2000 – 2001
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| Keywords | Renal cell carcinoma / VHL tumor suppressor gene / multicentiicity / comparative genomic hybridization |
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| Research Abstract |
The clonality of sporadic multiple renal cell carcinomas are unknown. We compared the genetic background of the multiple tumors by the mutation analyses of von Hippel Lindau (VHL) tumor suppressor gene. Furthermore, comparative genomic hybridization (CGH) was used to investigate genetic differences. The main tumor and the satellite tumor of four patients with renal cell carcinomas were investigated. In patient #1, no mutation of VHL gene was detected in the main tumor, however, missense mutation was detected in codon 167 (CGC→CCG; Arginme→Proline) in the satellite tumor. In patient #2, no mutation of VHL gene was detected in the main tumor, however, nonsense mutation was detected in codon 185 (TAC→TAG; Tyrosine→stop codon) in the satellite tumor. In patient #3, one base deletion was detected in codon 133 in the main tumor, however, no mutation of VHL gene was detected in the satellite tumor. In patient #4, no mutation of VHL gene was detected both in the main tumor and the satellite tumor, In summary, no common mutation in both the main and the satellite tumor was detected, which suggests clonality of multiple renal cell carcinomas are different. The result of the CGH supports the idea because common abnormality is rare between the main tumors and the satellite tumors.
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Research Products
(2 results)
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[Publications] Oya, M., Ohtsubo, M., Tkayanagi, A., Tachibana, M., Shimizu, N., Murai, M.: "Constitutive activation of nuclear factor-κB prevents TRAIL-induced apoptosis in renal cancer cells"Oncogene. 20. 3888-3896 (2001)
Description
「研究成果報告書概要(和文)」より
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