| Co-Investigator(Kenkyū-buntansha) |
SASAKI Motoko KANAZAWA UNIVERSITY,SECOND DEPARTMENT OF PATHOLOGY,ASSISTANT, 医学部, 助手 (70225895)
HOSO Masahiro KANAZAWA UNIVERSITY,SECOND DEPARTMENT OF PATHOLOGY,ASSISTANT, 医学部, 助手 (20219182)
SAITO Katsuhiko KANAZAWA UNIVERSITY,SECOND DEPARTMENT OF PATHOLOGY,ASSISTANT PROFESSOR, 医学部, 講師 (10205635)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 1994: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1993: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1992: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Research Abstract |
Recently, adenomatous hyperplasia (AH) of the human cirrhotic liver, which is a nodular lesion significantly larger (>8 mm) than the other regenerative nodules in the cirrhotic liver, has been regarded as a preneoplastic or early neoplastic lesion transforming to hepatocellular carcinoma (HCC), In this study, we investigated the histopathology, cell kinetics, cytoplasmic phenotypes and genetic changes of AH and HCC.AH was classifiable into ordinary AH and atypical AH.The former had no or little cellular atypia while the latter displayd moderate to severe cellular atypia not regarded as HCC.Atypical AH occasinally contained HCC foci, Clinical follow-up showed livers with atypical AH frequently develop HCC,while livers with ordinary AH did not. Cell kinetic study showed that cell proliferative activity was low in ordinary AH,moderate in atypical AH and severe in HCC.HCC foci within AAH showed high cell proliferative activity. With regard to cytoplasmic phenotypes, alpha-fetoproteins was
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negative in ordinary AH,infrequently positive in atypical AH and frequently positive in HCC.The HCC foci within atypical AH were occasionaly positive for alpha-fetoprotein. Capillarization of the sinusoids including changes in endothelia and presence of Ito cells and basement membrane was absent in ordinary AH,but was mildly present in atypical AH and markedly present in HCC.The number and luminal areas of arterial elements was low in ordinary AH,moderate in atypical AH and high in HCC.Cytokeratin 19-positive biliary cells was none in ordinary AH and HCC,but was present in atypical AH,suggesting that atypical AH can spread along bile ducts. P53 gene mutation was not present in AH,but infrequently present in HCC.K-ras mutation was inrfequently present in atypical AH,but frequently present in HCC.These data suggest that ordinary AH is not a preneoplastic lesion, but atypical AH is an important preneoplastic lesion leading to HCC.That is, human hepatocellular carcinogenesis at least in part progresses from atypical AH through atypical AH with HCC foci to HCC. Less
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