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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 | Augmented realitytrends in education: a systematic review of research andapplications显示文摘 | Bacca J Baldiris S Fabregat R | 2014 | Educational Technology & Society2014，17，4： | 1 |
| 5 | Surgical Resection of Colorectal Liver Metastases in Patients with Expanded Indications: A Single-Center Experience with 501 Patients显示文摘 | Juan Figueras M.D. Jaume Torras M.D. Carlos Valls M.D. Laura Llado M.D. Emilio Ramos M.D. Joan Marti-Ragué M.D. Teresa Serrano M.D. Juan Fabregat M.D | 2007 | Diseases of the Colon & Rectum2007，，4： | 1 |
| 6 | 查看详情显示文摘 | Alejandre A Medina F Salagre P Fabregat A.and Sueiras J.E | | 0，，： | 1 |
| 7 | Snail blocks the cell cycle and confers resistance to cell death显示文摘 | Vega S Morales AV Oca(n)a OH Valdés F Fabregat I Nieto MA | | 0，，10： | 1 |
| 8 | Increased expression of AQP 1 and AQP 5 in rat lungs ventilated with low tidal volume is time dependent 显示文摘 | Fabregat G Garc~a-de-la-Asunci6n J Sarri6 B | 2014 | PLoS One2014，9，14： | 1 |
| 9 | Molecular mechanisms of insulin resistance in IRS-2-deficient hepatocytes 显示文摘 | Valverde AM Burks DJ Fabregat I | 2003 | Diabetes2003，52，9： | 1 |
| 10 | Catalytic wet air oxidation of substituted phenols using activated carbon as catalyst显示文摘 | SUAREZ-OJEDA M E STUBER E FORTUNY A FABREGAT A CARRERA J FONT J | 2005 | Applied Catalysis BEnvironmental2005，58，12： | 1 |
| 11 | Solid pseudopapillary tumors of the pancreas:Diagnosis and curative treatment 显示文摘 | Frago R Fabregat J Jorba R | 2006 | Rev Esp Ebferm Dig2006，98，11： | 1 |
| 12 | Molecular mechanisms of insulin resistance in IRS-2-deficient hepatocytes 显示文摘 | Valverde A M Burks D J Fabregat I | 2003 | Diabetes2003，52，9： | 1 |
| 13 | Obstetric epidural analgesia and fetal heart rate:primum non nocere显示文摘 | Correa Chacon OC Fabregat Lopez J | 2010 | Minerva Anestesiol2010，76，4： | 1 |
| 14 | Molecular mechanisms of insulin resistance in IRS-2 deficient hepatocytes 显示文摘 | Valverde AM Burks DJ Fabregat I | 2003 | Diabetes2003，52，9： | 1 |
| 15 | Quantum dot polymethacrylate composites for the analysis of NO, by fluorescence spectroscopy 显示文摘 | FABREGAT V IZQUIERDO M A BURGUETE M I | 2012 | Inorganica Chimica Acta2012，381，15： | 1 |
| 16 | Outflow reconstruction with arterial patch in domino liver transplantation: a new technical option显示文摘Domino liver transplantation(LT), using livers from familial amyloidotic polyneuropathy(FAP) patients, is a well described technique useful to expand donor pool. One of the main difficulties of this type of LT arises from the necessity to share the vascular pedicles between the graft and the donor. The most important challenge resides in restoring a proper hepatic venous outflow in the FAP-liver recipient.This is specially challenging when using the piggy-back technique, because the hepatic stumps may be too short. To overcome this issue, surgeons explored several techniques using different types of venous grafts. We describe a new technical option by using an arterial graft from the deceased donor. By using both iliac arteries a long graft is created and sutured as needed to the hepatic vein stump. We describe herein this new technique employed in a domino liver recipient who underwent retransplantation for ischemic cholangitis. The procedure was performed using the piggy-back technique; the venous stump of the FAP liver was reconstructed with the arterial graft. The patient had uneventful postoperative and mid-term hepatic function, and anastomosis was patent 24 months after LT. | Laura Lladó Emilio Ramos Sofia De LaSerna Joan Fabregat | 2014 | Hepatobiliary & Pancreatic Diseases International2014，13，5： | 1 |
| 17 | Results of Treatment in Severe Acute Pancreatitis显示文摘 | POVES I FABREGAT J BIONDO S | 2000 | Rev Esp Enferm Dig2000，92，9： | 1 |
| 18 | Survival and apoptosis: a dysregulated balance in liver cancer 显示文摘 | Fabregat I Roncero C Fernandez M | 2007 | Liver International2007，27，2： | 1 |
| 19 | TGF-Beta signa- ling in cancer treatment显示文摘 | Fabregat I Fcrnmando J Mainez J | 2013 | Curr Pharm Des2013，12，： | 1 |
| 20 | Molecular mechanisms of insulin resistance in IRS-2-deficient hepatocytes显示文摘 | Valverde AM Burks DJ Fabregat I Fisher TL Carretero J White MF Benito M | 2003 | Diabetes2003，9，： | 1 |
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