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| 1 | Reactivation of the insulin-like growth factor-Ⅱsignaling pathway in human hepatocellular carcinoma显示文摘Constitutive activation of the insulin-like growth factor (IGF)-signaling axis is frequently observed in human hepatocellular carcinoma(HCC).Especially the over- expression of the fetal growth factor IGF-Ⅱ,IGF-Ⅰ receptor(IGF-IR),and cytoplasmic downstream effectors such as insulin-receptor substrates(IRS)contribute to proliferation,anti-apoptosis,and invasive behavior. This review focuses on the relevant alterations in this signaling pathway and independent in vivo models that support the central role IGF-Ⅱsignaling during HCC development and progression.Since this pathway has become the center of interest as a target for potential anti-cancer therapy in many types of malignancies,various experimental strategies have been developed,including neutralizing antibodies and selective receptor kinase inhibitors,with respect to the specific and efficient reduction of oncogenic IGF-Ⅱ/IGF-IR-signaling. | Kai Breuhahn Peter Schirmacher | 2008 | World Journal of Gastroenterology2008，14，11： | 40 |
| 2 | Nucleoporin 88 expression in hepatitis B and C virus-related liver diseases显示文摘AIM: To investigate the expression of nucleoporin 88 (Nup88) in hepatitis B virus (HBV) and C virus (HCV)-related liver diseases. METHODS: We generated a new monoclonal Nup88 antibody to investigate the Nup88 protein expression by immunohistochemistry (IHC) in 294 paraffin-embedded liver specimens comprising all stages of hepatocellular carcinogenesis. In addition, in cell culture experiments HBV-positive (HepG2.2.15 and HB611) and HBV-negative (HepG2) hepatoma cell lines were tested for the Nup88 expression by Western-immunoblotting to test data obtained by IHC.RESULTS: Specific Nup88 expression was found in chronic HCV hepatitis and unspecific chronic hepatitis, whereas no or very weak Nup88 expression was detected in normal liver. The Nup88 expression was markedly reduced or missing in mild chronic HBV infection and inversely correlated with HBcAg expression. Irrespective of the HBV- or HCV-status, increasing Nup88 expression was observed in cirrhosis and dysplastic nodules, and Nup88 was highly expressed in hepatocellular carcinomas. The intensity of Nup88 expression significantly increased during carcinogenesis (P < 0.0001) and correlated with dedifferentiation (P < 0.0001). Interestingly, Nup88 protein expression was significantly downregulated in HBV-positive HepG2.2.15 (P < 0.002) and HB611 (P < 0.001) cell lines as compared to HBV-negative HepG2 cells. CONCLUSION: Based on our immunohistochemical data, HBV and HCV are unlikely to influence the expression of Nup88 in cirrhotic and neoplastic liver tissue, but point to an interaction of HBV with the nuclear pore in chronic hepatitis. The expression of Nup88 in nonneoplastic liver tissue might reflect enhanced metabolic activity of the liver tissue. Our data strongly indicate a dichotomous role for Nup88 in non-neoplastic and neoplastic conditions of the liver. | Martina Knoess Anna Kordelia Kurz Olga Goreva Nuran Bektas Kai Breuhahn Magarethe Odenthal Peter Schirmacher Hans Peter Dienes C Thomas Bock Hanswalter Zentgraf Axel zur Hausen | 2006 | World Journal of Gastroenterology2006，12，36： | 4 |
| 3 | miR-615-5p is restrictedly expressed in cirrhotic and cancerous liver tissues and its overexpression alleviates the tumorigenic effects in hepatocellular carcinoma显示文摘 | H.M. El Tayebi K.A. Hosny G. Esmat K. Breuhahn Ahmed Ihab Abdelaziz | 2012 | FEBS Letters2012，，19： | 2 |
| 4 | Keratinocyte-derived granu- locyte-marophage colony stimulating factor accelerates wound healing: stimulation of ke ratinocyte proliferation,granul-ation tissue formation and vaseularization显示文摘 | Mann A Breuhahn K Schirmacher P | 2001 | J Invest Dermatol2001，117，6： | 1 |
| 5 | Beta-catenin accumulation in the progression of human hepatocarcinogenesis correlates with loss of E-cadherin and accumulation of p53,but not with expression of conventional WNT-1 target genes显示文摘 | Prange W Breuhahn K Fischer F | 2003 | J Pathol2003，201，2： | 1 |
| 6 | Analysis of UV-B modulared gene expression in human keratinocytes by mRNA differential display polymerase chain eaction显示文摘 | Abts H F Breuhahn K Michel G | 1997 | Photochem Photobiol1997，66，3： | 1 |
| 7 | Epidermal overexpression of granulocyte-macroph89e colony stimulating factor in duces both ker- atinocyte proliferation and apoptosis显示文摘 | Breuhahn K Mann A Muller G | 2000 | Cell Growth Differ2000，11，2： | 1 |
| 8 | Keratinocyte-derivedgranulocyte -macrophage colony stimulating factor accelerateswound healing: Stimulation of keratinocyte proliferation, granulationtissue formation, and vascularization 显示文摘 | Mann A Breuhahn K Schirmacher P | 2001 | J Invest Dermatol2001，117，6： | 1 |
| 9 | Factors of transforming growt h factor beta signalling are co-regulated in human hepatocellular carcinoma显示文摘 | Longerich T Breuhahn K Odenthal M | 2004 | Virchows Arch2004，445，6： | 1 |
| 10 | Chromosome aheralions in human hepatocellular carcinomas correlate with aetiology and histological grade-results of an explorative CGH meta-analysis显示文摘 | Moinzadeh P Breuhahn K Stuitzer H | 2005 | Br J Cancer2005，92，5： | 1 |
| 11 | Dysregu- lation of growth factor signaling in human hepatocellular carcino- ma显示文摘 | BREUHAHN K LONGERICH T SCHIRMACHER P | 2006 | Oncogene2006，25，27： | 1 |
| 12 | Molecular profiling of human hepatocellular carcinoma defines mutually exclusive interferon regu- lation and insulin-like growth factor II overexpression显示文摘 | Breuhahn K Vreden S Haddad R | 2004 | Cancer Res2004，64，17： | 1 |
| 13 | Keratinocyte- derived granulocyte-macrophage colony stimulating fac- tor accelerates wound healingstimulation of keratinocyte proliferation,granulation tissue formation, and vascular- ization 显示文摘 | Mann A Breuhahn K Sctirmacher P | 2001 | J Invest Dermatol2001，117，6： | 1 |
| 14 | Keratinocyte-de-rived granulocyte-macmphage colony stimulating factor acceler- ates wound healing: Stimulation of keratinoeyte proliferation, granulation tissue formation, and vascularization 显示文摘 | Mann A Breuhahn K Schirmacher P | 2001 | J Invest Dermatol2001，117，6： | 1 |
| 15 | 268 MIR-155 IS AN INDUCER FOR THE INSULIN-LIKE GROWTH FACTOR II MITOGENIC SIGNALING PATHWAY IN HCV-PROGRESSED HEPATOCELLULAR CARCINOMA显示文摘 | H.M. El Tayebi K.A. Hosny G. Esmat K. Breuhahn A.I. Abdelaziz | 2012 | Journal of Hepatology2012，，： | 1 |
| 16 | Inverse expression of Jun activation domain binding protein 1 and cell cycle inhibitor p27^Kip1: influence on proliferation in hepatocellular carcinoma显示文摘 | BERG JP ZHOU Q BREUHAHN K | 2007 | Human Pathology2007，38，11： | 1 |
| 17 | Molecular pro- filing of human hepatocellular carcinoma defines mutually exclusive interferon regulation and insulin - like growth factor overexpression 显示文摘 | Breuhahn K Vreden S Haddad R | 2004 | Cancer Res2004，64，9： | 1 |
| 18 | Epidermal overexpression of granulocyte-macrophage colony-stimulating factor induces both keratinocyte proliferation and apoptosis显示文摘 | Breuhahn K Mann A Muller G | 2000 | Cell Growth Differ2000，11，2： | 1 |
| 19 | Factors of transfor ming growth factor beta signalling are co-regulated in human hepatocellular carcinoma显示文摘 | Longerich T Breuhahn K Odenthal M | 2004 | Virchows Arch2004，445，6： | 1 |
| 20 | Factors of transform?ing growth factor beta signalling are co-regulated in human hepato?cellular carcinoma显示文摘 | Longerich T Breuhahn K Odenthal M | 2004 | Virchows Arch2004，445，6： | 1 |
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