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| 1 | Dysregulation of apoptosis in hepatocellular carcinoma cells显示文摘Hepatocellular carcinoma (HCC) is a major health problem, being the sixth most common cancer world-wide. Dysregulation of the balance between proliferation and cell death represents a pro-tumorigenic principle in human hepatocarcinogenesis. This review updates the recent relevant contributions reporting molecular alterations for HCC that induce an imbalance in the regulation of apoptosis. Alterations in the expression and/or activation of p53 are frequent in HCC cells, which confer on them resistance to chemotherapeutic drugs. Many HCCs are also insensitive to apoptosis induced either by death receptor ligands, such as FasL or TRAIL, or by transforming growth factor-beta (TGF-β). Although the expression of some pro-apoptotic genes is decreased, the balance between death and survival is dysregulated in HCC mainly due to overactivation of anti-apoptotic pathways. Indeed, some molecules involved in counteracting apoptosis, such as Bcl-XL, Mcl-1, c-IAP1, XIAP or survivin are over-expressed in HCC cells. Furthermore, some growth factors that mediate cell survival are upregulated in HCC, as well as the molecules involved in the machinery responsible for cleavage of their proforms to an active peptide. The expression and/or activation of the JAK/STAT, PI3K/AKT and RAS/ERKs pathways are enhanced in many HCC cells, conferring on them resistance to apoptotic stimuli. Finally, recent evidence indicates that inflammatory processes, as well as the epithelial-mesenchymal transitions that occur in HCC cells to facilitate their dissemination, are related to cell survival. Therefore, therapeutic strategies to selectively inhibit anti-apoptotic signals in liver tumor cells have the potential to provide powerful tools to treat HCC. | Isabel Fabregat | 2009 | World Journal of Gastroenterology2009，15，5： | 28 |
| 2 | Growth factor-and cytokine-driven pathways governing liver stemness and differentiation显示文摘Liver is unique in its capacity to regenerate in response to injury or tissue loss. Hepatocytes and other liver cells are able to proliferate and repopulate the liver. However, when this response is impaired, the contribution of hepatic progenitors becomes very relevant. Here, we present an update of recent studies on growth factors and cytokine-driven intracellular pathways that govern liver stem/pro-genitor cell expansion and differentiation, and the rel-evance of these signals in liver development, regeneration and carcinogenesis. Tyrosine kinase receptor signaling, in particular, c-Met, epidermal growth factor receptors or fibroblast growth factor receptors, contribute to prolifera-tion, survival and differentiation of liver stem/progenitor cells. Different evidence suggests a dual role for the trans-forming growth factor (TGF)-β signaling pathway in liver stemness and differentiation. On the one hand, TGF-βmediates progression of differentiation from a progenitor stage, but on the other hand, it contributes to the expan-sion of liver stem cells. Hedgehog family ligands are nec-essary to promote hepatoblast proliferation but need to be shut off to permit subsequent hepatoblast differentiation. In the same line, the Wnt family and β-catenin/T-cell fac-tor pathway is clearly involved in the maintenance of liver stemness phenotype, and its repression is necessary for liver differentiation during development. Collectively, data indicate that liver stem/progenitor cells follow their own rules and regulations. The same signals that are essential for their activation, expansion and differentiation are good candidates to contribute, under adequate conditions, to the paradigm of transformation from a pro-regenerative to a pro-tumorigenic role. From a clinical perspective, this is a fundamental issue for liver stem/progenitor cell-based therapies. | Aránzazu Sánchez Isabel Fabregat | 2010 | World Journal of Gastroenterology2010，16，41： | 7 |
| 3 | Role of the tissue microenvironment as a therapeutic target in hepatocellular carcinoma显示文摘Hepatocellular carcinoma is difficult to treat,primarilybecause the underlying molecular mechanisms drivingclinical outcome are still poorly understood.Growingevidence suggests that the tissue microenvironmenthas a role in the biological behavior of the tumor.Themain clinical issue is to identify the best target fortherapeutic approaches.Here,we discuss the hypothesis that the entire tissue microenvironment might beconsidered as a biological target.However,the tissuemicroenvironment consists of several cellular and biochemical components,each of which displays a distinctbiological activity.We discuss the major components ofthis environment and consider how they may interactto promote tumor/host crosstalk. | Bhavna Rani Yuan Cao Andrea Malfettone Ciprian Tomuleasa Isabel Fabregat Gianluigi Giannelli | 2014 | World Journal of Gastroenterology2014，20，15： | 6 |
| 4 | Autocrine production of TGF-β confers resistance to apoptosis after an epithelial–mesenchymal transition process in hepatocytes: Role of EGF receptor ligands显示文摘 | Gaelle del Castillo Miguel M. Murillo Alberto álvarez-Barrientos Esther Bertran Margarita Fernández Aránzazu Sánchez Isabel Fabregat | 2006 | Experimental Cell Research2006，，15： | 1 |
| 5 | SJWD14121100000298显示文摘 | Joan Fernando Andrea Malfettone Edgar B. Cepeda Roser Vilarrasa‐Blasi Esther Bertran Giulia Raimondi àngels Fabra Alberto Alvarez‐Barrientos Pedro Fernández‐Salguero Conrado M. Fernández‐Rodríguez Gianluigi Giannelli Patricia Sancho Isabel Fabregat | 2015 | Cancer2015，，4： | 1 |
| 6 | Supported Cu(II) polymer catalysts for aqueous phenol oxidation显示文摘 | Castro Isabel U Stuber Frank Fabregat Azael | 2009 | Journal of Hazardous Materials2009，163，2： | 1 |
| 7 | Supported Cu(Ⅱ) polymer catalysts for aqueous phenol oxidation显示文摘 | Castro Isabel U Stuber Frank Fabregat Azael | 2009 | Journal of Hazardous Materials2009，163，23： | 1 |
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