Molecular Characteristics of Fibrolamellar Hepatocellular Carcinoma
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  • 作者:Attila Patonai (1)
    Boglárka Erdélyi-Belle (1)
    Anna Korompay (1)
    áron Somorácz (1)
    Péter T?rzs?k (1)
    Ilona Kovalszky (2)
    Tamás Barbai (1)
    Erzsébet Rásó (1)
    Gábor Lotz (1)
    Zsuzsa Schaff (1)
    András Kiss (1)
  • 关键词:Fibrolamellar hepatocellular carcinoma ; Hepatocellular carcinoma ; Cholangiocellular carcinoma ; Epidermal growth factor receptor ; K ; RAS mutation
  • 刊名:Pathology & Oncology Research
  • 出版年:2013
  • 出版时间:January 2013
  • 年:2013
  • 卷:19
  • 期:1
  • 页码:63-70
  • 全文大小:713KB
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    3. Liu S, Chan KW, Wang B, Qiao L (2009) Fibrolamellar hepatocellular carcinoma. Am J Gastroenterol 104:2617-624 dx.doi.org/10.1038/ajg.2009.440">CrossRef
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    6. Patonai A, Erdélyi-Belle B, Korompay A, Somorácz á, Straub BK, Schirmacher P, Kovalszky I, Lotz G, Kiss A, Schaff Z (2011) Claudins and tricellulin in fibrolamellar hepatocellular carcinoma. Virchows Arch 458:679-88 dx.doi.org/10.1007/s00428-011-1077-y">CrossRef
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    19. Li W, Tan D, Zenali MJ, Brown RE (2010) Constitutive activation of nuclear factor- kappa B (NF-kB) signaling pathway in fibrolamellar hepatocellular carcinoma. Int J Clin Exp Pathol 3:238-43
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    21. Roskams T, De Vos R, Van Damme DG, Desmet V (1998) Heparan sulphate proteoglycan expression in primary liver tumors. J Pathol 185:190-97 dx.doi.org/10.1002/(SICI)1096-9896(199807)185:3<290::AID-PATH91>3.0.CO;2-I">CrossRef
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  • 作者单位:Attila Patonai (1)
    Boglárka Erdélyi-Belle (1)
    Anna Korompay (1)
    áron Somorácz (1)
    Péter T?rzs?k (1)
    Ilona Kovalszky (2)
    Tamás Barbai (1)
    Erzsébet Rásó (1)
    Gábor Lotz (1)
    Zsuzsa Schaff (1)
    András Kiss (1)

    1. 2nd Department of Pathology, Semmelweis University Budapest, üll?i út 93, 1091, Budapest, Hungary
    2. First Institute of Pathology and Experimental Cancer Research, Semmelweis University Budapest, Budapest, Hungary
  • ISSN:1532-2807
文摘
Fibrolamellar hepatocellular carcinoma (FLC) occurs in non-cirrhotic liver and the etiopathogenesis is still obscure. Both hepatocellular and cholangiocellular markers are expressed in the tumor, however, molecular alterations and altered pathways playing role in the tumor pathogenesis are not clearly identified. The purpose of the present study was to compare the expression level of EGFR, syndecan-1 and ?-catenin in FLC, conventional hepatocellular carcinoma (cHCC) and cholangiocellular carcinoma (CCC) and to investigate the possibility of mutation both in EGFR and K-RAS. Eight FLCs were compared with 7 cHCCs, 7 CCCs and 5 normal liver samples. Cytokeratins 7, 8, 18, 19, HepPar1 (HSA), EGFR, syndecan-1 (CD138) and ?-catenin were detected by immunohistochemistry. In addition EGFR, ?-catenin and syndecan-1 were evaluated by digital morphometry and K-RAS, EGFR mutations in FLC cases using paraffin-embedded samples. All FLCs were positive for HepPar1 (HSA) and cytokeratins 7, 8, 18, but negative for cytokeratin 19 by immunohistochemistry. EGFR was significantly overexpressed in all three tumor types, being highest in FLCs (p--,0001). EGFR, K-RAS mutation analyses revealed no mutations in exons studied in FLCs. Our findings proved that expression of EGFR is higher in FLC than in other types of primary malignant hepatic tumors and no K-RAS mutation can be detected, so FLC is a good candidate for anti-EGFR treatment.

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