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        <identifier>oai:niigata-u.repo.nii.ac.jp:00022876</identifier>
        <datestamp>2022-12-15T03:53:11Z</datestamp>
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          <dc:title>7) B型肝炎ウイルスの肝細胞癌発症機構(シンポジウム 遺伝子工学による病因解析とその診断, 第435回新潟医学会)</dc:title>
          <dc:title xml:lang="en">7) B型肝炎ウイルスの肝細胞癌発症機構(シンポジウム 遺伝子工学による病因解析とその診断, 第435回新潟医学会)</dc:title>
          <dcterms:alternative>A Mechanistic Role of Hepatitis B Virus in the Development of Hepatocellular Carcinoma(Molecular Genetic Approaches to Human Diseases)</dcterms:alternative>
          <jpcoar:creator>
            <jpcoar:creatorName>小方, 則夫</jpcoar:creatorName>
          </jpcoar:creator>
          <jpcoar:subject subjectScheme="Other">hepatitis B virus (HBV) carrier</jpcoar:subject>
          <jpcoar:subject subjectScheme="Other">hepatocellular carcinoma</jpcoar:subject>
          <jpcoar:subject subjectScheme="Other">HBV DNA integration</jpcoar:subject>
          <jpcoar:subject subjectScheme="Other">B型肝炎ウイルス（HBV）キャリア</jpcoar:subject>
          <jpcoar:subject subjectScheme="Other">肝細胞癌</jpcoar:subject>
          <jpcoar:subject subjectScheme="Other">HBV DNA組込み</jpcoar:subject>
          <datacite:description descriptionType="Abstract">We have previously described that 1) integration of hepatitis B virus (HBV) DNA into host chromosomes of hepatocytes occurs at a high frequency during the course of the viral carrier state, 2) hepatocytes containing the integrated viral DNA undergo multiclonal growth, and 3) all hepatocellular carcinomas (HCCs) develop clonally and some HCCs are of multiclonal origins even in a same liver. These findings indicate that HBV related HCC may be established through several steps of genetic alterations after the initial integration event of the viral DNA. To investigate the critical mode of HBV DNA integration for the transforming process of hepatocyte, we analyzed a HCC case for the structure of the integrants in both hepatocytes and hepatoma cell using molecular cloning technique. Characteristic features of the integrant found in the hepatoma cell were 1) the cohesive end region of HBV DNA along with flanking cellular DNA showed inverted repeat structure, and 2) the integration sites in host DNA was within human highly repetitive sequence, alpha satellite DNA. Results described were discussed from a viewpoint of a possible role of HBV in hepatocarcinogenesis.</datacite:description>
          <dc:publisher>新潟医学会</dc:publisher>
          <datacite:date dateType="Issued">1989-06</datacite:date>
          <dc:language>jpn</dc:language>
          <dc:type rdf:resource="http://purl.org/coar/resource_type/c_6501">departmental bulletin paper</dc:type>
          <jpcoar:identifier identifierType="HDL">http://hdl.handle.net/10191/41296</jpcoar:identifier>
          <jpcoar:identifier identifierType="URI">https://niigata-u.repo.nii.ac.jp/records/22876</jpcoar:identifier>
          <jpcoar:sourceIdentifier identifierType="NCID">AN00182415</jpcoar:sourceIdentifier>
          <jpcoar:sourceIdentifier identifierType="ISSN">00290440</jpcoar:sourceIdentifier>
          <jpcoar:sourceTitle>新潟医学会雑誌</jpcoar:sourceTitle>
          <jpcoar:sourceTitle xml:lang="en">新潟医学会雑誌</jpcoar:sourceTitle>
          <jpcoar:volume>103</jpcoar:volume>
          <jpcoar:issue>6</jpcoar:issue>
          <jpcoar:pageStart>466</jpcoar:pageStart>
          <jpcoar:pageEnd>471</jpcoar:pageEnd>
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            <datacite:date dateType="Available">2019-08-19</datacite:date>
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