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1995 Fiscal Year Final Research Report Summary

THE STUDY OF ONCOGENE,TUMOR SUPPRESSER GENE AND HEPATITIS VIRUS GENNES RELATED TO HEPATOCELLULAR CARCINOMA

Research Project

Project/Area Number 06670555
Research Category

Grant-in-Aid for General Scientific Research (C)

Allocation TypeSingle-year Grants
Research Field Gastroenterology
Research InstitutionOKAYAMA UNIVERSITY

Principal Investigator

YUMOTO Yasuhiro  Okayama University ISOTOPE CENTER,ASSOCIATE PROFESSOR, アイソトープ総合センター, 助教授 (30033369)

Co-Investigator(Kenkyū-buntansha) KOIDE Norio  OKAYAMA UNIVERSITY MEDICAL SCHOOL HOSPITAL,DOCENT, 医学部・附属病院, 講師 (20142333)
HANAFUSA Tadashi  OKAYAMA UNIVERSITY ISOTOPE CENTER,ASISTANT PROFESSOR, アイソトープ総合センター, 助手 (00228511)
Project Period (FY) 1994 – 1995
KeywordsHepatocellular carcinoma, / Tumor suppresser gene, / p53, / LOH, / RB, / HBV, / HCV, / RLGS, / AP-PCRSSCP
Research Abstract

The mechanisms of development of HCC is still unclear the examination of genetic changes in tumor suppresser genes and oncogenes should be a valuable to elucidate the mechanisms of carcinogenesis. Frequent allelic losses at loci on chromosomes 4q, 5q, 11p, 13q, and 17p have been reported. Eighty percents of patients analyzed had been exposed to hepatitis B virus (HBV) and/or hepatitis C virus (HCV). The frequenciea of LOH on seven chromosomes were 57.9% in 17p13.3,45.1% in 17p, 45.1% in 11p, 41.9% in5q, 41.9% in 16q24,29.0% in 4q, 25.8% in advanced HCCs (4 of well differentiated, 18 of moderately differentiated and of poorly differentiated carcinoma). On the contrary LOH was observed on 4q, 5q, 16q, and 17p in 33% (1/3) of the small HCCs (2 of well differentiated, and one of moderately differentiated carcinoma). The mutation of the p53 genes and polymorphism of the RB gene were presen in 25.8% (8/31) and 12.9% (4/31) of the advanced tumor respectively, but the mutation was not found in … More small HCC.LOH on every chromosome and p53 mutation were observed more frequently in more advanced tumors, and the genetic changes accumulated with the increase of the histological grade. These findings suggest that the of genetic changes in multiple tumor suppresser genes are involved in the progression of HCC.
We examined mutations of p53 by PCR-SSCP analysis and the configuration of HBV by genetic southern hybridization in 39 HCC tissues. Although there was no statistical significance, the frequency of the mutations of p53 in HBs antigen-positive negative samples (three of 15 (20%)) was slightly lower than that HBs antigen samples (seven of 16 (44%)). The mutations were detected in HCCs that have integrated HBV DNA (three of 10) and on HBV DNA (eight of 22), but was not detected in the HCCs which had free HBV (none of seven). These observations suggested that p53 and the HBV replication are associated with the development of HCC.Polymorphism of the RB gene were present in 25.8% (8/31) and 12.9% (4/31) of the advanced tumor respectively, but the mutation was not found in small HCC.LOH on every chromosome and p53 mutation were observed more frequently in more advanced tumors, and the genetic changes accumulated with the increase of the histological grade. These findings suggest that the accumulation of genetic changes in multiple tumor suppresser genes are involved in the progression of HCC.
We examined mutations of p53 by PCR-SSCP analysis and the configuration of HBV by genetic southern hybridization in 39 HCC tissues. Although there was no statistical significance, the frequency of the mutations of p53 in HBs antig (three of 15 (20%) was slightly lower than that in HBs antigen negative samples (seven The mutations were detected in HCCs that have integrated HBV DNA (three of 10) and no HBV DNA eight of 22) but was not detected in the HCCs which had free HBV (none of seven) These observations suggested that p53 and the HBV replication are associated with the developm HCC.Alteration of genomic DNAs in HCCs were examined by restriction landmark genomic scanning (RLGS) and AP-PCR-SSCP analysis. Five spots were more intense in 10-14 in the 16HCCs (63-88%). The intensity of several spots was reduced to about half, suggesting the loss of one of two alleles.. the use of landmarks that show a reproducible increase or decrease in intensity is discussed in conjunction with future studies of genomic alteration inherent in HCC. Less

  • Research Products

    (15 results)

All Other

All Publications (15 results)

  • [Publications] Yumoto Y, Hanafusa T, etal: "Loss of fieterozygo sity and Analysis of mutation of p53 in hepato cellular carcinoma" J. Gastroenterology and Hepatology. 10. 179-185 (1995)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Yumoto Y, Mitani T. etal: "Preoperativl estimation of remnant liver function before hapatectomy using 99 TC GSA" Seninar in Oncobogy. (inpress). (1996)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Tamura T,Koide N, etal: "Gene expression of the liner specific proteins, albumin and trans ferin, in well corlserbd in hepatocyle" Acta Med Okayama. 49. 161-167 (1995)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Hirasaki S, Koide N: "A family with hereditary serum clrolinesterase deficiency." Internal Meolicine. 34. 632-635 (1995)

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      「研究成果報告書概要(和文)」より
  • [Publications] Sasaki S, Koide N et al: "Immunohilochemical study of prateoglycans in d-galactosamine-induced acute hopatilis in rat." Gasboenterology. 31. 46-54 (1996)

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      「研究成果報告書概要(和文)」より
  • [Publications] Shiraha H,KoideN et al: "Improvement of serum amino acid profile in hepatic failure voith the bio-srtificidl liver icsing nwiticellular hepatocyte spheroids" Biotechnalogy & bioengineering. (impress). (1996)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] 湯本 泰浩, 辻 孝夫: "わかりやすい消化管疾患基礎編・消化器癌の腫瘍マーカー" 杏林書院 岩崎 有良, 沖田 極 他編, 14 (1996)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Yumoto Y,Hanafusa T,Hada H,Ooguchi S,Shinji T,Mitani T,Koide N,and Takao T: "Loss of heterozygosity and analysis of Mutation of p53 in hepatocellular carcinoma." J,Gastroenterology Hepatology. 10. 179-185 (1995)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Yumoto Y,Umeda M,Ohshima K,Ogawa H,Kurose T,T,anand Tsuji T.: "Estimation of remnant hepatic function by" Cancer Chemotherapy and Pharmacology. 33. 1-6 (1994)

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      「研究成果報告書概要(欧文)」より
  • [Publications] Nagai H,Ponglikitmongkol M,Mita E,Ohmachi Y,Yoshikawa H,Yumoto Y,Nakanishi T,and Matsubara K.: "Aberration of gnomic DNA in association with human hepatocellular carcinoma detected 2-dimensional gel analysis." Cancer Research. 54. 1545-1550 (1994)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Yumoto Y,Mitani T,Koide N,Hada H,Umeda M,Kurokawa K,and Tshuji T.: "Preoperative estimation of remnant liver function before hepatectomy using Tc-99m-GSA." Seminar in Oncology 1996. (in press).

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Tamura T,Koide N,and Tsuji T.: "Gene expression of the liver specific proteins., albumin and transferring in well conserved in hepatocyte spheroid." Acta Med Okayama. 49(3). 161-167 (1995)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Sasaki H,Koide N,and Tsuji T.: "Immunohistochemical study of proteoglycanes in galactosamine induced acute hepatitis in rats." J of Gastroenterology. 31. 46-54 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Shiraha H,Koide N,and Tsuji T.: "Improvement of serum amino acid profile in hepatic failure with the bioartificial liver using multicellular hepatocyte spheroids." Biotechnology and Bioengineering 1996. (in.

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Yumoto Y and Tsuji T.: "Tumor markers in gastrointestinal organ." Basic Gastroentelogy Editor Okita Kiwamu Kyourin Shoin Tokyo. (1996)

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Published: 1997-03-04  

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