| Project/Area Number |
05671051
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Digestive surgery
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| Research Institution | NIIGATA NIVERSITY |
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Principal Investigator |
SUZUKI Tsutomu Niigata University School of Medicine The First Department of Surgery Associate Professor, 医学部, 助教授 (40183420)
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| Co-Investigator(Kenkyū-buntansha) |
AIZAWA Kikuo Niigata University School of Medicine University Hospital The First Department o, 医学部・附属病院, 助手 (10222449)
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| Project Period (FY) |
1993 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1995: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1994: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1993: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | Cancer Metastasis / Genetic Instability / DNA Recombinational Mutation / DNA Fingerprint / Minisatellite DNA / Patient Prognosis / p53遺伝子 / 癌転移能 / 遺伝子組み換え変異 / SSCP法 |
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| Research Abstract |
The aim of this study was to investigate the significance of the DNA recombinational mutation based on the genetic instability and the p53 gene mutation in the development of metastatic potential in human cancer cells. Peripheral white blood cells (Wbc), tumor tissue and normal colonic mucosa were obtained from 4 patients undergoing colectomy for an advanced colorectal cancer. DNA were extracted from the materials and prepared to examine the DNA recombinational mutation with DNA fingerprinting by Southern hybridization technique. The hPc-1, a polymorphic minisatellite probe, was used to detect mutations. As to the p53 gene mutation, aterials were sampled from 7 patients and prepared for anlysis using th single strand confor-mation polymorphisms technique (SSCP) . The exon 6 was focused to examine the presence of mutation.
The 4 cancer specimens exhibited no extra-bands resulting from recombination and/or DNA slippage as compared to the corresponding Wbc and normal mucosa. The 7 cancer specimens did not show any mutations either as to the exon 6. These nay resulted from inadequately small number of specimens (patients) and also, presumably, inappropriate analytic methodolgy for human materials. We consider the accumulation of subject materials and modification of assay systems.
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