tbuckley/cabot-search huggingface dataset:
Very high real-world efficacy of ritonavir boosted paritaprevir with ombitasvir and dasabuvir +/− ribavirin in hepatitis C genotype 1 in patients with advanced fibrosis –Final results of the REV1TAL study
Authors: J.S. Lubel, S. Pianko, A. Thompson, S. Strasser, G. Dore, K. Stuart, G. MacQuillan, D. Iser, J. Mitchell, A. Gazzola, S. Chivers, G. Mishra, P. Gow, J. George, J. Gough, E. Tse, A. Zekry, M. Levy, V. Fragomeli, B. Morales, J. Sasadeusz, S. Nazareth, S. Bollipo, T. Jones, A. Wade, W. Cheng, A. Wigg, S. Roberts
Journal: Journal of Hepatology (2017)
Correlation of expressions of ER/PR/HER-2 receptor status with clinicopathological parameters in Mauritian breast cancer patients.
Authors: Shyam Shunker Manraj, Nilufer Jasmine Selimah Fauzee, Urvashee Ramsamy, Meera Manraj, Anil Bhushan Mohith
Journal: Journal of Clinical Oncology (2015)

e11536 Background: Breast cancer is by far the commonest site of cancer registered in Mauritius with an ASR of 56.0/105 in females. This study intends to correlate the expressions of HER-2, estrogen receptor (ER) and progesterone receptor (PR) with clinicopathological parameters in breast carcinoma. It is in fact the ever first study of its kind to be carried out in the Mauritian context. Methods: A prospective study was conducted during a period of two years (2013-2014) at the Central Health Laboratory, Victoria Hospital; whereby 78 paraffin blocks of consecutive breast cancer cases diagnosed were subjected to ER/ PR testing by immunohistochemistry (IHC). As regards to HER-2 testing, they were sent to Lancet laboratories, South Africa for IHC. Chi-Square test was used to evaluate IHC results with prognostic parameters for breast cancer. Results: In the present study, 77 were females and 1 was male; the mean age of patients was 52.7 years ranging from 26 to 80 years, 33 patients (42.3%) were below 50 years of age. 52 cases had defined menopausal status, 67.3% were post-menopausal and 32.7% were pre-menopausal. Infiltrating ductal carcinoma (NOS) was the commonest 48/78 (61.5%) and the other variants 30/78 (38.5%). The overall immunoexpression of ER/PR/HER-2 were 73.6%, 61.8%, 35.9% respectively; HER-2 was overexpressed (3+) in 23.3% of cases and triple negative cases accounted for 17.9%. In terms of laterality, we found that right breast was slightly more involved (53.9%) than left breast (46.2%). ER/PR positivity was associated with Lymph node involvement with marginal significance (p = 0.074). No significant association was found between ER/PR/HER2 as well as with age, tumor size and grade. Conclusions: There are high rates of positive expressions of ER/PR/HER-2/neu among the Mauritian population with breast carcinoma. This year the Central Health Laboratory is planning to set up a comprehensive IHC service with on-site testing for HER-2; hence further studies are to be anticipated on the topic.
Ductular reactions provide a structural biliary network to preserve bile drainage in the CDE-model of hepatocellular chronic liver injury
Authors: L.-A. Clerbaux, R. Manco, N. Van Hul, R. Español-Suñer, C. Bouzin, C. Sempoux, N. Theise, I. Leclercq
Journal: Journal of Hepatology (2017)
Bacterial deoxyribonucleic is frequent in blood samples of patients with compensated cirrhosis and obesity and is associated with lack of decrease of portal pressure after an intensive lifestyle intervention
Authors: R. Francés, A. Albillos, C. Villanueva, J. Genescá, A. Ardevol, S. Augustín, J.L. Calleja, R. Bañares, J.C. García-Pagán, F. Mesonero, J. Bosch, A. Beragotti
Journal: Journal of Hepatology (2017)
Linkage to care of HBsAg and anti-HCV positive patients after a systematic screening approach in the German primary care setting
Authors: A. Lüllau, D. Petroff, O. Bätz, J. Kramer, K. Jedrysiak, H. Tenckhoff, T. Berg, I. Wolffram, J. Wiegand
Journal: Journal of Hepatology (2017)
Risk Associated With Complications and Mortality After Urgent Surgery vs Elective and Emergency Surgery
Authors: Matthew G. Mullen, Alex D. Michaels, J. Hunter Mehaffey, Christopher A. Guidry, Florence E. Turrentine, Traci L. Hedrick, Charles M. Friel
Journal: JAMA Surgery (2017)

Given the current climate of outcomes-driven quality reporting, it is critical to appropriately risk stratify patients using standardized metrics.To elucidate the risk associated with urgent surgery on complications and mortality after general surgical procedures.This retrospective review used the American College of Surgeons National Surgery Quality Improvement Program database to capture all general surgery cases performed at 435 hospitals nationwide between January 1, 2013, and December 31, 2013. Data analysis was performed from November 11, 2015, to February 16, 2017.Any operations coded as both nonelective and nonemergency were designated into a novel category titled urgent.The primary outcome was 30-day mortality; secondary outcomes included 30-day rates of complications, reoperation, and readmission in urgent cases compared with both elective and emergency cases.Of 173 643 patients undergoing general surgery (101 632 females and 72 011 males), 130 235 (75.0%) were categorized as elective, 22 592 (13.0%) as emergency, and 20 816 (12.0%) as nonelective and nonemergency. When controlling for standard American College of Surgeons National Surgery Quality Improvement Program preoperative risk factors, with elective surgery as the reference value, the 3 groups had significantly distinct odds ratios (ORs) of experiencing any complication (urgent surgery: OR, 1.38; 95% CI, 1.30-1.45; P < .001; and emergency surgery: OR, 1.65; 95% CI, 1.55-1.76; P < .001) and of mortality (urgent surgery: OR, 2.32; 95% CI, 2.00-2.68; P < .001; and emergency surgery: OR, 2.91; 95% CI, 2.48-3.41; P < .001). Surgical procedures performed urgently had a 12.3% rate of morbidity (n = 2560) and a 2.3% rate of mortality (n = 471).This study highlights the need for improved risk stratification on the basis of urgency because operations performed urgently have distinct rates of morbidity and mortality compared with procedures performed either electively or emergently. Because we tie quality outcomes to reimbursement, such a category should improve predictive models and more accurately reflect the quality and value of care provided by surgeons who do not have traditional elective practices.
Multimutational profiling of rebiopsy samples from NSCLC developing acquired resistance to EGFR-TKI in Japanese patients.
Authors: Ryo Ko, Hirotsugu Kenmotsu, Masakuni Serizawa, Yasuhiro Koh, Shota Omori, Kazuhisa Nakashima, Takuya Oyakawa, Kazushige Wakuda, Yasushi Hisamatsu, Akira Ono, Hisao Imai, Tetsuhiko Taira, Tateaki Naito, Haruyasu Murakami, Mitsuhiro Isaka, Masahiro Endo, Takashi Nakajima, Yasuhisa Ohde, Nobuyuki Yamamoto, Toshiaki Takahashi
Journal: Journal of Clinical Oncology (2014)

e19032 Background: The majority of non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations eventually acquire resistance to EGFR tyrosine kinase inhibitors (TKI). There are little data about genetic alterations in rebiopsy samples of NSCLC developing acquired resistance to EGFR-TKI in Asian patients. Methods: We retrospectively reviewed the medical records of patients with NSCLC harboring EGFR mutations, who had undergone rebiopsy after acquired resistance to EGFR-TKI. We analyzed 30 practicable samples using our tumor genotyping panel to assess 23 hot-spot sites of genetic alterations in 9 genes (EGFR, KRAS, BRAF, PIK3CA, NRAS, MEK1, AKT1, PTEN and HER2), gene copy number of EGFR, MET, PIK3CA, FGFR1 and FGFR2, and ALK, ROS1 and RET fusions using pyrosequensing plus capillary electrophoresis, quantitative PCR, and reverse transcription PCR, respectively. In addition, 23 samples were analyzed by commercially available EGFR mutation tests (Cycleave PCR or Scorpion Amplification Refractory Mutation System). Acquired resistance was defined according to Jackman's criteria. Results: A total of 43 patients had undergone rebiopsy and analysis of resistance mechanisms. Thirty rebiopsy samples were analyzed using our tumor genotyping panel, and 13 rebiopsy samples were analyzed for EGFR mutations only by commercial clinical laboratories. Anatomic sites of rebiopsy were 28 thoracic lesions, 10 central nervous system lesions, and 5 other lesions. Eleven patients (26%) had second-site EGFR T790M mutations, and 4 patients had no EGFR activating mutations in rebiopsy samples. No patients had small cell histologic transformation. In samples analyzed using our tumor genotyping panel, MET gene copy number gain was seen in 3 of 30 (10%). In addition, we detected PIK3CA mutation (E542K), PIK3CA gene copy number gain, BRAF mutation (G466V), and KRASmutation (G12D), in one sample each. Genetic alterations were identified in 36% of central nerve system samples, and 53% of other samples. Conclusions: Althoughfrequency of T790M mutation was lower than earlier reports for western patients, that of MET gene copy number gain was comparable to previous reports.
Delisting of liver transplant candidates with chronic hepatitis C virus infection after viral eradication: outcome after delisting: a European study
Authors: L.S. Belli, M. Berenguer, P.A. Cortesi, R. Facchetti, M. Strazzabosco, G. Perricone, S.-R. Rockenschaub, S. Martini, C. Morelli, F. Donato, R. Volpes, G.-P. Pageaux, A. Coilly, S. Fagiuoli, G. Berlakovich, S. Monico, C. Vinaixa, W. Polak, C. Duvoux
Journal: Journal of Hepatology (2017)
CCAAT/Enhancer Binding Protein Delta exerts tumor-supportive effects but is down-regulated in patient hepatocellular carcinoma
Authors: P. Liu, W. Cao, B.Y. Ma, K. Chen, K. Sideras, J. Duitman, M. Bolkestein, R. Smits, A. Spek, J. Kwekkeboom, M. Peppelenbosch, Q. Pan
Journal: Journal of Hepatology (2017)
Further delineation of fibrosis progression in NAFLD: evidence from a large cohort of patients with sequential biopsies
Authors: S. Mcpherson, R. Pais, L. Valenti, J.M. Schattenberg, J.-F. Dufour, E. Tsochatzis, S. Francque, T. Hardy, M. Boyle, D. Tiniakos, V. Ratziu, Q. Anstee
Journal: Journal of Hepatology (2017)
A Meta-Analysis of Clinical Trials on the Risk of Hyponatraemia in Cancer Patients Treated with Targeted Therapies
Authors: R Berardi, S Rinaldi, M Santoni, E Nunzi, A Smerilli, M Caramanti, F Morgese, M Torniai, A Onofri, M Pistelli, A Taccaliti, S Cascinu
Journal: Journal of Thoracic Oncology (2015)
Recurrent noncoding regulatory mutations in pancreatic ductal adenocarcinoma
Authors: Michael E Feigin, Tyler Garvin, Peter Bailey, Nicola Waddell, David K Chang, David R Kelley, Shimin Shuai, Steven Gallinger, John D McPherson, Sean M Grimmond, Ekta Khurana, Lincoln D Stein, Andrew V Biankin, Michael C Schatz, David A Tuveson
Journal: Nature Genetics (2017)
Abstract 36: Disrupting the Delta Protein Kinase C Interaction with the “d” Subunit of F1Fo ATP Synthase Protects Against Ischemia-Reperfusion Injury in Perfused Rat Hearts
Authors: John A Johnson, Mourad Ogbi, Robert W Caldwell
Journal: Circulation Research (2012)

Cardiac ischemia / reperfusion (IR) injury is associated with severe energy deprivation and is the number one cause of death world-wide. Mitochondrial F1Fo ATP synthase produces &gt;90% of cardiac energy in mammals, yet few studies have targeted its role in IR injury. Previously, we identified a hypoxia-induced interaction of delta protein kinase C (dPKC) with the “d” subunit of F1Fo ATP synthase (dF1Fo) in neonatal cardiac myocytes, which inhibits F1Fo function. In the present work we investigated the hypothesis that a novel peptide inhibitor of the dPKC-dF1Fo interaction would preserve ATP and reduce infarct-size in isolated rat hearts subjected to IR injury. This peptide [NH2-YGRKKRRQRRRMLATRALSLIGKRAISTSVC-COOH] contains HIV-Tat protein transduction and mitochondrial targeting domains, the dPKC-dF1Fo inhibitor sequence, and a FLAG epitope. In hearts exposed to global ischemia, or IR, dPKC co-immuno-precipitated with dF1Fo. Pretreatment with the dPKC-dF1Fo inhibitor exacerbated cardiac ATP loss by 1.9-fold (n=5, p&lt;0.03) following 10 min of global ischemia. However; following a pro-longed IR exposure ATP levels were enhanced by 2.1-fold (p&lt;0.02, n=5). These opposing effects of the[[Unable to Display Character: ]]dPKC-dF1Fo inhibitor on ATP levels are likely due to relief of dPKC inhibition of the different modes of the F1Fo complex during ischemia (ATPase) and oxygenated reperfusion (ATP synthase). We next used 2,3,5, tetrazolium chloride staining techniques to determine if the dPKC-dF1Fo inhibitor had infarct-sparing effects following prolonged IR. In hearts exposed to 30 min of global ischemia and 150 min of reperfusion the dPKC-dF1Fo inhibitor reduced infarct size, (expressed as the percentage of total LV area) from 45 + 3 % (n=6) to 22 + 3 % (n=6, p &lt; 0.01). Delivery and stability of the dPKC-dF1Fo inhibitor in hearts was confirmed by FLAG immunoreactivity in western blots conducted on mitochondria isolated the left ventricle. This is the first demonstration that perfusion with the dPKC-dF1Fo inhibitor prior to IR improves ATP recovery and reduces infarction in intact mammalian hearts. Our results support the potential for this peptide as a first-in-class translational agent for combating cardiac IR injury.
A pospective study to evaluate the impact of early everolimus on the recurrence of hepatocellular carcinoma after liver transplantation
Authors: M. Rodríguez-Perálvarez, M. Guerrero, L. Barrera, G. Ferrín, J.M. Alamo, D. Ayllón, G. Suarez, J.L. Montero, J. Briceño, J. Padillo, E. Fraga, E. Perea, J.M. Pascasio, M.A. Gómez-Bravo, M. De la Mata
Journal: Journal of Hepatology (2017)
Myeloid-Derived Suppressor Cells: key players mediating immunosuppression via induction of Regulatory T-cell by TGFβ and IL-10 driven pathways in chronic HBV infection
Authors: S. Pal, M. Nandi, D. Dey, S.M. Ahammed, S. Banerjee, A. Santra, A. Chowdhury, S. Datta
Journal: Journal of Hepatology (2017)
Allelic variantes of Aurora B kinase gene can be related with fibrosis progression in chronic hepatitis C
Authors: I. Francisco-Recuero, A.I. Gil, A. Madejón, A. Sánchez-Pacheco, M. Romero, A. García, A. Olveira, P. Castillo, J.C. Erdonzaín, C. Perales, E. Domingo, R. Mena, J. García-Samaniego
Journal: Journal of Hepatology (2017)
Abstract B39: Asparagine drives translational adaptation of cancer cells to glutamine deficit
Authors: Natalya N. Pavlova, Ji Zhang, Craig B. Thompson
Journal: Cancer Research (2017)

Abstract Most proliferating cells consume exogenous glutamine to fuel biosynthesis and cell growth, which leads to its marked depletion from the microenvironment. Glutamine provides carbon and nitrogen for a wide array of biomolecules, among which are non-essential amino acids, glucosamine and nucleotides; in addition, carbon backbone of glutamine is used as a preferred anaplerotic input into the TCA cycle. However, as recent in vivo metabolomic studies indicate, a number of tumor types are capable of utilizing alternative anaplerotic routes and, in fact, synthesize glutamine de novo. In addition, select cancer cell lines are able to proliferate in the absence of exogenous glutamine in culture medium. However, the metabolic and regulatory underpinnings that enable the cellular adaptation to glutamine deficit and de novo glutamine production need further investigation. In this work, we identified the non-essential amino acid asparagine as essential for the survival and proliferation of cancer cells in the absence of exogenous glutamine supply. Our data indicate that asparagine, though structurally related to glutamine, is not catabolized in the same manner. Instead, asparagine acts by restoring protein translation, which becomes profoundly compromised in the absence of glutamine. This, in turn, enables the post-transcriptional adaptive upregulation of glutamine synthetase (GLUL), which is required for glutamine-independent growth. Taken together, these findings show that the cellular adaptation to glutamine-limiting conditions relies upon the availability of asparagine, which may represent an important therapeutic vulnerability. Citation Format: Natalya N. Pavlova, Ji Zhang, Craig B. Thompson. Asparagine drives translational adaptation of cancer cells to glutamine deficit. [abstract]. In: Proceedings of the AACR Special Conference on Translational Control of Cancer: A New Frontier in Cancer Biology and Therapy; 2016 Oct 27-30; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2017;77(6 Suppl):Abstract nr B39.
For publication in the European Respiratory Journal
Authors: J. Hedner, L. Grote, M. Bonsignore, W. McNicholas, P. Lavie, G. Parati, P. Sliwinski, F. Barbé, P. Escourrou, I. Fietze, J.F. Masa, J.A. Kvamme, C. Lombardi, O. Marrone, J.M. Montserrat, T. Penzel, M. Pretl, R. Riha, D. Rodenstein, T. Saaresranta, R. Schulz, R. Tkacova, G. Varoneckas, A. Vitols, H. Vrints, J. Zielinski, W DeBacker
Journal: European Respiratory Journal (2011)

The European Sleep Apnoea Database (ESADA) reflects a network of 22 sleep disorder centres in Europe enabled by a COST action B26 program. This ongoing project aims to describe differences in standard clinical care of patients with obstructive sleep apnoea (OSA) and to establish a resource for genetic research in this disorder.

Patients with suspected OSA are consecutively included and followed up according to local clinical standards. Anthropometrics, medical history, medication, daytime symptoms and sleep data (polysomnography or cardiorespiratory polygraphy) are recorded in a structured web-based report form.

5103 patients (1426 females, age 51.8±12.6 years, 79.4% with AHI≥5 events·hr−1) were included from March 15, 2007 to August 1, 2009. Morbid obesity (BMI≥35 kg·m−2) was present in 21.1% of males and 28.6% of women. Cardiovascular, metabolic, and pulmonary comorbidities were frequent (49.1, 32.9 and 14.2%, respectively). Patients investigated with a polygraphic method had a lower AHI than those undergoing polysomnography (23.2±23.5 vs. 29.1±26.3 events·hour−1, p<0.0001).

The ESADA is a rapidly growing multicentric patient cohort that enables unique outcome research opportunities and genotyping. The first cross sectional analysis reveals a high prevalence of cardiovascular and metabolic morbidity in patients investigated for OSAS.
Advancing age and comorbidities in chronic hepatitis B patients: results of 10-year longitudinal analysis of a diverse population-based cohort of 44,026 chronic hepatitis B patients in the United States
Authors: M.H. Nguyen, J. Lim, A.B. Ozbay, J. Fraysse, I. Liou, N. Meyer, G. Dusheiko, S. Gordon
Journal: Journal of Hepatology (2017)
[11C]Choline-PET imaging of breast cancer
Authors: L. M. Kenny, R. C. Coombes, K. Contractor, J. Stebbing, A. Al-Nahhas, C. Palmieri, S. Shousha, C. Lowdell, E. Aboagye
Journal: Journal of Clinical Oncology (2009)

1110 Background: Molecular imaging techniques are increasingly being used in cancer diagnosis, staging, and assessment of response to treatment. This study sought to evaluate, for the first time, [ 11 C]choline-PET in patients with breast cancer. The potential of [ 11 C]choline-PET for differentiating tumours from normal tissue, correlation with molecular markers, determine its normal variability range, and finally the effect of trastuzumab on [ 11 C]choline uptake in patients with breast cancer was investigated. Methods: 21 patients with newly diagnosed and recurrent breast cancer AJCC stage II-IV were enrolled in the study, all of whom had a baseline dynamic [ 11 C]choline-PET scan with arterial sampling. 14 patients had 2 [ 11 C]choline-PET scans to examine reproducibility, and 7 had a scan after trastuzumab. Analysis of [ 11 C]choline uptake was measured using SUV, Ki (irreversible retention), and IRF@60min (retention using spectral analysis). Results: Breast tumour lesions were visualised by [ 11 C]choline PET in all patients. The difference in tumour and non-tumour uptake were significant for SUV, Ki, and IRF@60 min (Wilcoxon p &lt; 0.0001 for all parameters). [ 11 C]choline uptake was reproducible in breast tumour lesions (r 2 = 0.945 for SUV, 0.894 for Ki, and 0.799 for IRF60). The metabolism analysis of arterial plasma samples in 19 patients showed that [ 11 C]choline decreased rapidly post-injection such that at 60 mins the mean radioactivity in arterial plasma due to choline was 15.15 ± 2.16%.Early responses to trastuzumab were determined to be significant in 5 lesions which corresponded with 3 clinical responses. Conclusions: [ 11 C]choline-PET is a promising imaging modality in breast cancer, and could play an important role for determining response to novel treatment strategies in vivo. No significant financial relationships to disclose.
Anti-Fibrotic Effect of Autotaxin and LPA1R Antagonists in a Rodent Model of NASH.
Authors: Malavi Madireddi, Gretchen Bain, James Swaney, Brian Murphy, Simeon Taylor
Journal: Hepatology (2015)

Anti-Fibrotic Effect of Autotaxin and LPA1R Antagonists in a Rodent Model of NASH.: 141  Malavi Madireddi;Gretchen Bain;James Swaney;Brian Murphy;Simeon Taylor; Hepatology
Abstract 028: CCN1 Enables Fas Ligand-Induced Apoptosis by Elevating Fas Expression in Primary Cardiomyocytes or by Increasing Cytoplasmic Smac in Cardiomyoblast H9c2 Cells
Authors: Bor-Chyuan Su, Fan-E Mo
Journal: Circulation Research (2013)

Fas/Fas ligand (FasL) is implicated in cardiac ischemia/reperfusion injury. However, cardiomyocytes in culture are resistant to FasL-induced apoptosis, suggesting that additional factor(s) are required for FasL-induced apoptosis. Matricellular protein CCN1 has been demonstrated to promote cytotoxicity of FasL in human skin fibroblasts. CCN1 is induced in a variety of cardiac pathologies. We assessed the hypothesis that CCN1 may be involved in the regulation of FasL-induced apoptosis in cardiomyocytes. We found that either FasL or CCN1 did not induce cell death in neonatal rat ventricular cardiomyocytes (NRVM). Interestingly, the combination of FasL+CCN1 generated 2-fold induction of apoptosis (vs. control p&lt;0.001). An integrin-α 6 β 1 -binding defective mutant CCN1, CCN1-DM failed to exert synergy with FasL to induce apoptosis, indicating a critical role of α 6 β 1 . The engagement between CCN1 and α 6 β 1 instigated the elevation of cellular reactive oxygen species (ROS), the activation of mitogen activated protein kinase p38, and followed by the induction of cell surface display of Fas, thereby sensitizing NRVM to FasL-induced apoptosis. Pretreatment of the p38 inhibitor SB202190 abolished the CCN1-induced cell-surface Fas expression and the apoptosis induced by FasL+CCN1. In addition, we tested the interaction between CCN1 and FasL on the cardiomyoblast H9c2 cells. We found that FasL or CCN1 alone did not cause apoptosis in H9c2, and required the combination of FasL+CCN1 to induced apoptosis (vs. control p&lt;0.001) in H9c2 cells, reminiscent of the observation in NRVM. Mechanistically, CCN1 acted through binding to integrin α 6 β 1 , ROS generation, and p38 activation, however, did not increase the expression of cell surface Fas for its synergy with FasL in H9c2 cells. Instead, CCN1 induced Bax translocation to mitochondria, which in turn led to the release of Smac from mitochondria to cytosol. The cytosolic Smac functions to neutralize XIAP. Smac is critical for CCN1 action, because the knockdown of Smac blunted the apoptotic activities of CCN1. In conclusion, CCN1 may play a detrimental role in a stressed heart to both the differentiated cardiomyocytes and the proliferative cardioblasts through distinct signaling mechanisms.
THE TRANS–STENOTIC PRESSURE GRADIENT DURING THE DIASTOLIC WAVE–FREE PERIOD IS PROPORTIONAL TO FLOW: THE PHYSIOLOGICAL BASIS OF THE INSTANT–WAVE–FREE RATIO
Authors: Sayan Sen, Ricardo Petraco, Sukhjinder Nijjer, Rodney Foale, Iqbal Malik, Ghada Mikail, Alun Hughes, Javier Escaned, darrel francis, Jamil Mayet, Justin Davies
Journal: Journal of the American College of Cardiology (2013)
Identification of actionable mutations in circulating cell-free tumour DNA as a prognostic biomarker in hepatocellular carcinoma
Authors: J. Howell, S. Atkinson, D.J. PInato, S. Knapp, C. Ward, R. Minisini, M. Burlone, M. Leutner, M. Pirisi, S. Khan, M. Odenthal, M. Thursz, R. Sharma
Journal: Journal of Hepatology (2017)