tbuckley/cabot-search huggingface dataset:
A phase 1 trial of vandetanib (multikinase inhibitor of EGFR, VEGFR, and RET) in combination with everolimus (mTOR inhibitor) in patients with advanced malignancies.
Authors: Manojkumar Bupathi, Gerald Steven Falchook, David S. Hong, Ishwaria Mohan Subbiah, Sarina Anne Piha-Paul, Daniel D. Karp, Babita Saigal, Ralph Zinner, Jennifer J. Wheler, Apostolia Maria Tsimberidou, Siqing Fu, Steven I. Sherman, Funda Meric-Bernstam, Vivek Subbiah
Journal: Journal of Clinical Oncology (2014)

TPS2639 Background: Preclinical models have shown that concurrent inhibition of the mammalian target of rapamycin (mTOR) pathway signaling cooperates with epidermal growth factor (EGFR)/vascular endothelial growth factor (VEGFR) and RET inhibitors to overcome primary and / or acquired resistance to tumors sensitive and resistant to anti-EGFR/VEGFR/RET inhibitors. EGFR, VEGF, RET and mTOR are validated targets in numerous malignancies. Tumor responses induced by these single agents are transient and patients can develop secondary resistance. The predominant mechanism underlying resistance to these agents is unknown but likely due to activation of several concomitant pathways. Therefore, multi-kinase targeting of EGFR, VEGFR and mTOR may improve results compared to either agent alone. Based on this hypothesis, we are conducting an investigator initiated phase I trial combining vandetanib and everolimus for patients with advanced malignancies. Methods: This is a phase I dose escalation and expansion trial with a conventional “3+3” design. During the escalation phase, vandetanib and everolimus were given at the following respective doses: level 0 (100 mg, 2.5 mg), level 1 (200mg, 2.5mg), level 2 (200mg, 5mg), level 3 (300 mg, 5mg), and level 4 (300mg, 10mg). The inclusion criterion includes any patient with advanced cancer which is refractory to standard therapy, relapsed after standard therapy, or those who have no standard therapy options. Both study drugs are given continuously on a 28 day schedule. Dose adjustments for everolimus were done if patients were on CYP3A4 inducers or inhibitors so that appropriate serum concentration is reached. At this time all dose levels have been completed and the study is in a dose expansion phase. Dose expansion is being done in patients with genomic alternations in RET, EGFR, VEGFR, KDR, or P13K,PIK3R1, TSC1/2 and AKT aberrations and patients with tumor types for which vandetanib or everolimus is individually FDA approved. Clinical trial information: NCT01582191.
Dynamic alterations of the mTOR-Raptor-4EBP1-eIF4E complex during myogenesis of C2C12 myoblasts
Authors: Lili Shu, Peter Houghton
Journal: Cancer Research (2005)

Proc Amer Assoc Cancer Res, Volume 46, 2005

1505 

Differentiation of skeletal muscle cells involves three major steps, namely, withdrawal of myoblasts from the cell cycle, subsequent expression of myotube-specific genes, and formation of multinucleated myotubes. Previous study has shown that proliferation is mediated by the Raf/MEK/ERK pathway, whereas differentiation is mediated by the PI3K/AKT/mTOR pathway. However, exactly why mTOR signaling is essential in myogenic differentiation remains obscure though rapamycin, a very specific inhibitor of mTOR signaling, inhibits myogenic differentiation in C2C12 myoblasts. In cells mTOR is thought to exist in a large complex (> 1 megaDa) with several proteins including Raptor and GβL, and possibly other proteins. Previous studies reported that Raptor binds to mTOR though HEAT regions and binds to 4EBP1 through C terminal TOS motif of 4EBP1 to regulate the mTOR pathway. However, it is unknown whether mTOR complexes are regulated during myogenic differentiation. In this study we have analyzed complexes associated with eIF4E under conditions of growth (growth medium, GM) or differentiation (differentiation medium, DM). Under both conditions eIF4E binds to 7-methyl-GTP-sepharose-4B resin, and can be readily isolated. Using this ‘pull-down’ technique we have analyzed proteins bound to eIF4E under GM and DM conditions. Raptor and 4EBP1 were associated with eIF4E in both GM and DM. Rapamycin increased the association 4EBP1 as anticipated, but not raptor. Interestingly, when C2C12 cells were cultured in GM, 4EBP1 and Raptor were associated with eIF4E, but mTOR was rarely detected in the complex with antibody 26E3. When C2C12 cells were cultured in DM for 24 hrs, mTOR was strongly detected in the eIF4E complex.The results suggest a conformational change during early differentiation that yields tighter binding of mTOR to Raptor. Under nutrient restriction (low amino acids), raptor binds more tightly to mTOR and inhibits mTOR-dependent signaling (Kim et al. Cell 110:163, 2002). To determine whether the mTOR-Raptor complex induced under DM conditions also inhibited signaling, we examined the phosphorylation of two downstream targets of mTOR, p70S6K (Thr389) and 4EBP1 (Thr37). In contrast to the effect of amino acid deficiency, mTOR signaling is not inhibited in differentiating myoblasts. The results suggest that the affinity of mTOR-Raptor-4EBP1-eIF4E interactions increases during myogenic differentiation, and may be be essential for terminal differentiation. Based on these data, we propose that in C2C12 myoblasts there is a dynamic change in mTOR-Raptor-4EBP1-eIF4E complexes associated with cell cycle withdrawal. Other proteins may be involved in the regulation, such as g-actin, which was found associated with the complex in rapamycin-treated cells. The exact relation between the dynamics of these complexes and regulation of myogenesis is under further study. Supported by CA7776, CA96696 and ALSAC
High serum human beta-defensin-1 is associated with increased short-term mortality in patients with decompensated cirrhosis
Authors: D. Agiasotelli, A. Alexopoulou, L. Vasilieva, I. Mani, E. Hadziyannis, D. Goukos, G.L. Daikos, S.P. Dourakis
Journal: Journal of Hepatology (2017)
Effectiveness and safety of sofosbuvir-based regimens for Japanese patients with hepatitis C virus genotype 1b or 2 infection: real life experience from a multicenter cohort
Authors: E. Ogawa, N. Furusyo, H. Nomura, K. Dohmen, N. Higashi, K. Takahashi, A. Kawano, K. Azuma, T. Satoh, M. Nakamuta, T. Koyanagi, S. Shimoda, M. Kato, E. Kajiwara, J. Hayashi
Journal: Journal of Hepatology (2017)
Growth arrest by sulfasalazine (SASP) of subrenal capsule prostate cancer xenografts in immuno-deficient mice is coupled to a decrease in the number of tumor-associated macrophages
Authors: Peter W. Gout, Takeshi Kurita, Daniel Doxsee, Hui Xue, Yuzhuo Wang
Journal: Cancer Research (2005)

5865  SASP is an established anti-inflammatory drug which at low levels (0.2 mM) specifically inhibits cellular cystine uptake mediated by the xc- plasma membrane cystine transporter. As such, SASP can be used to arrest proliferation of cancer cells which critically depend for growth on extracellular cystine (or cysteine, the reduced form). We have previously shown that SASP can arrest growth of lymphoma cells via cyst(e)ine starvation by inhibiting (i) their uptake of cystine via the xc- transporter and (ii) secretion of cysteine, an xc--mediated process, by fibroblasts in their environment acting as cysteine suppliers. Notably, intraperitoneal administration of SASP to rats markedly inhibited growth of lymphoma transplants (Anti-Cancer Drugs 14:21, 2003). Further studies aimed at prostate cancer showed that DU-145 and PC3 human prostate cancer cells have a critical requirement for extracellular cystine, in contrast to LNCaP cells capable of synthesizing cysteine. As expected, LNCaP cells were much less sensitive in vitro to SASP-induced growth arrest than DU-145 and PC3 cells. In the present study, the response of LNCaP xenografts in immuno-deficient mice to treatment with SASP was compared with that of DU-145 and PC3 tumors. Groups of male, testosterone-supplemented Rag-2M mice were used, carrying established LNCaP cell xenografts (about 80 mm3) under the kidney capsules. Every 12 h they received i.p. injections of saline (controls; n=4) or SASP (250 mg/kg body wt; n=7) for 8 days. Animals were then sacrificed and tumors harvested for volume measurement and histological analysis (H&E and macrophage staining, using biotinylated, rat antimouse macrophage antibodies). It was found that LNCaP xenografts were surprisingly sensitive to SASP treatment, showing growth arrests of about 70% (relative to controls), comparable to growth arrests found for DU-145 and PC3 tumors. Immunohistochemical analysis revealed presence in control mice of numerous mouse macrophages lining tumor-kidney boundaries. In contrast, the numbers of such tumor-associated macrophages (TAMs) were markedly reduced in SASP-treated mice. Administration of SASP (i.p.) has been reported to decrease numbers of mouse macrophages. Taken together, the results suggest that the growth arrest of LNCaP tumors by SASP may be due to a reduction in the number of TAMs and consequently their tumor growth-promoting activity, recently recognized as an important factor in cancer development. In the case of DU-145 and PC3 tumors, a reduction in immunologically activated TAMs would likely also lead to decreased cysteine supply. SASP, an old drug, may be useful in prostate cancer therapy for targeting tumor growth-promoting macrophages. Supported by CIHR and DOD US Army.
A phase II trial of gemcitabine and docetaxel in hormone-refractory metastatic prostate cancer
Authors: S. Thakkar, T. Hutson, J. Garcia, J. Rothaermal, M. Bart, R. Dreicer
Journal: Journal of Clinical Oncology (2006)

14501 Background: Docetaxel is a microtubule stabilizing agent with demonstrated ability to improve survival in patients (pts) with hormone refractory metastatic prostate cancer (HRMPC). Gemcitabine is a nucleoside analogue that exhibits broad antitumor activity, although as a single agent has modest activity in advanced prostate cancer. The combination of docetaxel and gemcitabine has demonstrated significant activity in a variety of chemotherapy resistant neoplasms. We performed a phase II study of this combination to assess its safety and antitumor activity in chemotherapy naïve patients with HRMPC. Methods: Eligible pts had HRMPC with radiologic and/or biochemical evidence of progression following antiandrogen withdrawal with castrate testosterone levels, ECOG PS 0–2 and adequate organ function; no prior chemotherapy was permitted. Gemcitabine (800 mg/m 2 ) was administered on days 1 and 8 and docetaxel (75mg/m 2 ) on day 8 every 21 days for a maximum of 6 cycles. Results: Twenty-nine pts have been enrolled to date with 22 currently evaluable for response, all are evaluable for toxicity. The median age was 68. The average number of cycles completed was 4.9. Nine pts have experienced grade 4 neutropenia (1 neutropenic fever admission). Twelve of 29 pts have required dose delays secondary to wbc or platelets, two pts have required dose modification. Non-hematologic grade 3/4 toxicities include 1 pt with a PE, 1 grade 4 dyspnea, 1 grade 4 GI bleed. Four pts (18%) achieved measurable disease + PSA, partial response (PR), 7 (32%) additional pts had &gt;50% decline in PSA, for a composite overall response rate of 50%. Conclusions: The combination of gemcitabine and docetaxel is moderately toxic primarily impacting bone marrow reserve. Although there is evidence of significant antitumor activity, the ulitmiate utility of this doublet remains undefined. Accrual to this study is ongoing. [Table: see text]
Changes in the lipid profile in hepatitis C virus infected patients treated with direct-acting antivirals
Authors: L. Monteserín, R. Quiñones, G. Molina, M. Guerra, E. Fernández-Morán, M. Jiménez, N. Reyes, B. Álvarez-Cuenllas, P. Linares, S. Vivas, E. Gutiérrez, F. Jorquera
Journal: Journal of Hepatology (2017)
Extracellular Vesicles in Angiogenesis
Authors: Dilyana Todorova, Stéphanie Simoncini, Romaric Lacroix, Florence Sabatier, Françoise Dignat-George
Journal: Circulation Research (2017)

During the past decade, extracellular vesicles (EVs), which include apoptotic bodies, microvesicles, and exosomes, have emerged as important players in cell-to-cell communication in normal physiology and pathological conditions. EVs encapsulate and convey various bioactive molecules that are further transmitted to neighboring or more distant cells, where they induce various signaling cascades. The message delivered to the target cells is dependent on EV composition, which, in turn, is determined by the cell of origin and the surrounding microenvironment during EV biogenesis. Among their multifaceted role in the modulation of biological responses, the involvement of EVs in vascular development, growth, and maturation has been widely documented and their potential therapeutic application in regenerative medicine or angiogenesis-related diseases is drawing increasing interest. EVs derived from various cell types have the potential to deliver complex information to endothelial cells and to induce either pro- or antiangiogenic signaling. As dynamic systems, in response to changes in the microenvironment, EVs adapt their cargo composition to fine-tune the process of blood vessel formation. This article reviews the current knowledge on the role of microvesicles and exosomes from various cellular origins in angiogenesis, with a particular emphasis on the underlying mechanisms, and discusses the main challenges and prerequisites for their therapeutic applications.
Transarterial infusion of epirubicin and cisplatin combined with systemic infusion of 5-FU for advanced hepatocellular carcinoma refractory to conventional transarterial Infusion with doxorubicin
Authors: H.J. Kim, Y.W. Kim, J.H. Kwon, S.W. Nam, J.Y. Lee, J.W. Jang, K.W. Chung
Journal: Journal of Hepatology (2017)
Close association of arrest-defective protein 1 (ARD1) overexpression with frequent postoperative recurrence and poor survival in patients with hepatocellular carcinoma
Authors: D. Lee, H.J. Kang, Y.-H. Chung, G.H. Choi, J.H. Seo, J.-H. Park, H.S. Lee, J. Choi, M.-K. Jang, S.H. Ryu, Y.J. Lee, E. Yu, K.-W. Kim
Journal: Journal of Hepatology (2017)
Europium‐Doped Cerium Oxide Nanoparticles Limit Reactive Oxygen Species Formation and Ameliorate Intestinal Ischemia–Reperfusion Injury
Authors: Ekaterina O. Gubernatorova, Xiaobo Liu, Ali Othman, Wayne T. Muraoka, Ekaterina P. Koroleva, Silvana Andreescu, Alexei V. Tumanov
Journal: Advanced Healthcare Materials (2017)

Accumulating evidence suggests that ischemia–reperfusion‐induced injury is associated with the formation of reactive oxygen species (ROS). This study demonstrates the therapeutic effectiveness of novel europium‐doped cerium oxide nanoparticles (Eu‐doped Ceria NPs) as ROS scavengers in a mouse model of intestinal ischemia–reperfusion‐induced injury. An increased production of superoxide radicals is detected in the intestine throughout the ischemia stage and again after initiating reperfusion. These changes in superoxide radical formation are associated with the induction of inflammatory cytokines in the intestine. This study further shows that Eu‐Ceria NPs exhibit superoxide scavenging activity in vitro. Importantly, administration of Eu‐Ceria NPs into the intestinal lumen during the onset of ischemia effectively blocks superoxide accumulation, reduces the expression of IL‐1b, and ameliorates the intestinal pathology. These results suggest that early increased production of ROS during the ischemia–reperfusion promotes intestinal pathology and that mucosal delivery of Eu‐Ceria NPs may be a potential therapeutic approach to block ROS accumulation and ameliorate the severity of intestinal disease.
Effect of metformin versus placebo on weight and metabolic factors in initial patients enrolled onto NCIC CTG MA.32, a multicenter adjuvant randomized controlled trial in early-stage breast cancer (BC).
Authors: Pamela Jean Goodwin, Wendy Parulekar, Karen A. Gelmon, Lois E. Shepherd, Jennifer A. Ligibel, Dawn L. Hershman, Priya Rastogi, Ingrid A. Mayer, Timothy J. Hobday, Julie Lemieux, Alastair Mark Thompson, Kathleen I. Pritchard, Timothy Joseph Whelan, Som Dave Mukherjee, Haji I. Chalchal, Conrad D. Oja, Katia Sonia Tonkin, Vanessa Bernstein, Bingshu E Chen, Vuk Stambolic
Journal: Journal of Clinical Oncology (2013)

1033 Background: MA.32 investigates effects of Metformin vs. Placebo, in addition to standard care, on invasive disease free survival and other outcomes. Metformin may improve obesity and metabolic factors [insulin, glucose, leptin, C-reactive protein (CRP)] that have been associated with poor BC outcomes. Maintaining blinding of investigators to outcomes, we conducted a planned, DSMB approved, analysis of the effect of Metformin vs. Placebo on weight and metabolic factors at 6 months, including examination of interactions with baseline body mass index (BMI), in the first 498 subjects with paired fasting plasma samples. Methods: 498 non-diabetic subjects with T1-3, N0-3, M0 BC meeting defined entry criteria who had completed surgery and adjuvant chemo (if given) provided fasting blood samples at randomization and 6 months (while on study drug). Glucose was measured locally; blood was aliquoted, frozen and stored at -80°C then shipped to NCIC CTG (Kingston, Canada). Paired plasma aliquots were shipped to Mount Sinai Hospital (Toronto, Canada) for analysis of Insulin (Dako), hsCRP (Roche Elecsys) and leptin (Luminex). Statistical analysis used the Wilcoxon signed rank test. Results: Mean age was 52.4 ±9.2 years. Arms were balanced for ER/PgR (63% pos), BMI, prior adjuvant chemo (89%), T and N status, grade, mastectomy/lumpectomy and radiation. Conclusions: Metformin significantly improved weight, insulin, glucose, leptin and CRP at 6 months. Effects did not vary by baseline BMI. Funded by: NIH, CCSRI, CBCF, BCRF, Apotex Canada (drug &amp; placebo - in kind). Clinical trial information: NCT01101438. [Table: see text]
Impact of weight reduction on serum markers and liver histology including progression to cirrhosis in patients with nonalcoholic steatohepatitis (NASH) and bridging fibrosis
Authors: V. Ratziu, A. Sanyal, D. Torres, H. Hinrichsen, L. Serfaty, K. Bambha, S. Jayakumar, Z. Goodman, M. Abdelmalek, R. Aguilar, C. Jia, B. Mccolgan, R. Myers, M. Subramanian, J. McHutchison, N. Afdhal, S. Harrison
Journal: Journal of Hepatology (2017)
The old patient in DAA era: real life reports on 5925 patients from the Lombardy HCV Network
Authors: L. Pasulo, A. Aghemo, S. Fargion, A. Spinetti, G. Cologni, F. Maggiolo, G. Rizzardini, M. Puoti, R. Bruno, L. Minoli, M. Zuin, C. Uberti, T. Quirino, A.D. Monforte, A. Colli, M.G. Rumi, C. Iegri, S. Fagiuoli, M. Colombo
Journal: Journal of Hepatology (2017)
Interferon-free therapy is effective and safe for hepatitis C recurrence in liver transplant hepatitis C virus/human immunodeficiency virus coinfected recipients: a case-control study
Authors: M.-C. Londoño, C. Manzardo, S. Del Campo, L. Castells, V. Aguilera, J.R. Fernández, J. Calvo-Pulido, J. Peñafiel, A. Rimola, J.M. Miro
Journal: Journal of Hepatology (2017)
A novel non-invasive Golgi protein 73 (GP73)-based model accurately diagnoses significant fibrosis in chronic liver disease
Authors: Z. Cao, Z. Li, Y. Liu, R. Mo, P. Ren, L. Chen, J. Lu, Y. Zhuang, Y. Liu, X. Wang, G. Zhao, W. Tang, X. Xiang, H. Wang, W. Cai, Q. Xie
Journal: Journal of Hepatology (2017)
On-treatment decline in HBeAg level at week 24 predicts for HBeAg seroconversion during long-term tenofovir therapy for HBeAg-positive CHB
Authors: D. Wong, M. Littlejohn, L. Yuen, K. Jackson, H. Mason, A. Gaggar, K. Kitrinos, M. Subramanian, P. Marcellin, M. Buti, H. Janssen, E. Gane, J. Bayliss, V. Sozzi, D. Colledge, S. Locarnini, A. Thompson, P. Revill
Journal: Journal of Hepatology (2017)
Platelet microparticles infiltrating solid tumors transfer miRNAs that suppress tumor growth
Authors: James V. Michael, Jeremy G. T. Wurtzel, Guang Fen Mao, A. Koneti Rao, Mikhail A. Kolpakov, Abdelkarim Sabri, Nicholas E. Hoffman, Sudarsan Rajan, Dhanendra Tomar, Muniswamy Madesh, Marvin T. Nieman, Johnny Yu, Leonard C. Edelstein, Jesse W. Rowley, Andrew S. Weyrich, Lawrence E. Goldfinger
Journal: Blood (2017)
Simulated microgravity significantly impacts the differentiation and metabolism of human hepatic and biliary tree stem/progenitor cells
Authors: D. Costantini, V. Cardinale, L. Casadei, G. Carpino, L. Nevi, S. Di Matteo, A. Lustri, S. Safarikia, F. Melandro, P.B. Berloco, C. Manetti, D. Alvaro
Journal: Journal of Hepatology (2017)
Updated interim analysis of UCI 09-53: A phase II, single arm study of pazopanib and paclitaxel as first-line treatment for subjects with unresectable advanced melanoma.
Authors: Shlomit Y. Ein-Gal, Walter Tsang, Beverly Alger, Basmina Parmakhtiar, James G. Jakowatz, Claudette Bettis, John Fruehauf
Journal: Journal of Clinical Oncology (2013)

9082 Background: Metastatic melanoma lacks effective therapy. Pazopanib is an inhibitor of VEGFR-1,2,3, PDGFR-B and c-KIT that has antiangiogenic activity in renal cell cancer as well as inhibition of melanoma tumor xenografts. We designed a phase II single arm, open label clinical trial evaluating pazopanib in combination with metronomic paclitaxel as first line therapy for subjects with unresectable stage III and stage IV melanoma. Methods: This protocol utilizes a Simon 2-stage Minimax design, with a planned interim analysis to confirm &gt;3 responders to move to the second stage. To date, 31 patients are evaluable for response. All subjects were treatment naïve and received paclitaxel at 80mg/m2 weekly for three weeks in a 4 week cycle and pazopanib 800mg continuous daily oral dose. The primary endpoint is 6 month progression free survival. Exploratory endpoints include biomarker analysis that may be associated with treatment outcomes (serum VEGF, soluble VEGFR-2, serum HIF, serum TSP1 and BRAF mutation status). An additional exploratory endpoint includes the in vitro activity of pazopanib and paclitaxel on patient biopsy material co-cultured with vascular endothelial cells. RECIST 1.1 criteria were used to define treatment response (SD criteria was a minimum interval of 8 weeks). Results: For the 31 evaluable patients treated to date the following results were seen: 1 CR, 9 PR’s, 13 SD’s and 8 PD’s. The overall RR (CR+PR) was 32%. Total disease control rate was 74% (CR+PR+SD). The most common AEs/lab abnormalities were diarrhea (66%) nausea (60%), hypertension (63%), fatigue (63%) and vomiting (29%). Grade 3-4 AEs included hypertension (26%), transaminitis (23%) and neutropenia (17%).One patient discontinued for grade 4 transaminitis which subsequently resolved completely. Dose reductions were required for pazopanib in 15 patients and for paclitaxel in 4 patients. Conclusions: Updated interim analysis of this phase II study demonstrated that pazopanib in combination with paclitaxel was well tolerated and resulted in a 32% response rate, indicating that this combination is of further interest. Accrual will continue to reach a goal of 60 patients. Clinical trial information: NCT01107665.
How often do we misclassify alcoholic as nonalcoholic fatty liver disease due the subjectivity in assessing alcohol consumption?
Authors: M.V. Machado, S. Policarpo, D.P. Barreira, S. Carvalhana, J. Leitão, A.P. Silva, F. Velasco, I. Medeiros, C. Alves, M. Bourbon, H. Cortez-Pinto
Journal: Journal of Hepatology (2017)
Predicting Poor Overall Survival in Patients with Newly Diagnosed Multiple Myeloma and Standard-Risk Cytogenetics Treated with Novel Agents
Authors: Moritz Binder, S. Vincent Rajkumar, Rhett P. Ketterling, Angela Dispenzieri, Martha Q. Lacy, Morie A. Gertz, Francis K Buadi, Suzanne R. Hayman, Yi L. Hwa, Steven R. Zeldenrust, John A Lust, Stephen J. Russell, Nelson Leung, Prashant Kapoor, Ronald S. Go, Wilson I Gonsalves, Robert A. Kyle, Shaji K. Kumar
Journal: Blood (2016)
Excellent efficacy but increased rate of severe adverse events in HCV-infected elderly patients undergoing interferon-free therapy
Authors: S. Lens, I. Fernandez, S. Rodríguez-Tajes, M. Vergara, M. Forné, J.L. Calleja, M. Diago, J. Llaneras, S. Llerena, X. Torras, B. Sacristan, M. Roget, C.M. Fernández-Rodríguez, C. Navascués, J. Fuentes, J.J. Sanchez-Ruano, M.A. Simón, F. Saez-Royuela, C. Baliellas, R.M. Morillas, X. Forns
Journal: Journal of Hepatology (2017)