tbuckley/cabot-search huggingface dataset:
Abstract 12975: Electrocardiographic Left Ventricular Hypertrophy Predicts Atrial Fibrillation Independent of Left Ventricular Anatomy
Authors: Nikhil Patel, Wesley T O’Neal, S. P Whalen, Elsayed Z Soliman
Journal: Circulation (2016)

Introduction: It has been established that LVH detected by electrocardiography (ECG-LVH) and LVH detected by echocardiography (echo-LVH) carry different prognostic profiles in the prediction of cardiovascular disease events. It remains unclear whether ECG-LVH and echo-LVH are independently predictive of atrial fibrillation (AF). Methods: This analysis included 4,904 white participants (40% male; 85% white) aged 65 years or older from the Cardiovascular Health Study who were free of baseline AF and major intraventricular conduction defects. ECG-LVH was defined by Minnesota ECG Classification criteria from baseline ECG data. Echo-LVH was defined by sex-specific left ventricular mass values &gt;95th percentile for the study population. Incident AF events were identified during the annual study ECGs and from hospitalization discharge data. Cox regression was used to compute hazard ratios (HR) and 95% confidence intervals (CI) for the association of ECG-LVH and echo-LVH with adjudicated incident AF events, separately. Results: ECG-LVH was detected in 224 (4.6%) participants and echo-LVH was present in 231 (4.7%) participants. Over a median follow-up of 11.9 years, a total of 1,430 AF events were detected. In a multivariable Cox model adjusted for age, sex, race, education, income, body mass index, high-density lipoprotein cholesterol, total cholesterol, smoking, systolic blood pressure, diabetes, aspirin, antihypertensive medications, valve disease, coronary heart disease, and heart failure, ECG-LVH (HR=1.44; 95%CI=1.14, 1.83) and echo-LVH (HR=1.42; 95%CI=1.11, 1.82) were independently associated with AF. When ECG-LVH (HR=1.42, 95%CI=1.12, 1.80) and echo-LVH (HR=1.40, 1.09, 1.79) were included in the same model, both were predictive of incident AF. Conclusions: The association of ECG-LVH with AF is not dependent on abnormalities of left ventricular anatomy. These data suggest that abnormalities in cardiac electrophysiology provide a distinct profile in the prediction of AF.
Prostate Specific Membrane Antigen (PSMA): A prodrug target for prostate cancer
Authors: Stephen Alley, Michael Sun, Michael Torgov, Kevin Beam, Kevin Hamblett, Charles Cerveny, Joseph Francisco, Nathan Ihle, Peter Senter
Journal: Cancer Research (2004)

626  PSMA, a 100kDa type II membrane glycoprotein possesses a number of characteristics that make it a suitable candidate for prostate cancer specific therapy. PSMA expression is highly restricted to prostate tissue with strongest expression in both primary and metastatic prostate cancers and PSMA expression is upregulated upon androgen withdrawal. The extracellular domain of PSMA is accessible to agents in the extracellular peri-tumoral fluid thus making it possible to target prodrugs for enzymatic activation. Two discrete enzymatic functions for PSMA have been described. PSMA harbors the hydrolytic properties of N-acetylated alpha-linked acidic dipeptidase ( NAALADase) and is able to hydrolyze the neuropeptide N-acetyl-aspartyl-l-glutamate (NAAG). In addition, PSMA also functions as a pteroyl poly-gamma-glutamyl carboxypeptidase (folate hydrolase) and is able to progressively hydrolyze gamma glutamyl linkages of both poly gamma glutamated folates and methotrexate analogs with varying length glutamate chains. In order to develop prodrugs that can be activated within prostate cancers by PSMA’s enzymatic activity, a PSMA specific peptide carrier is required. In the present study a number of peptide substrates in which the amino acid portion consisted primarily of alpha or gamma carboxyl linked glutamic and or aspartic acids of various chain lengths were coupled to the amino terminus of 8-O-(12Aminododecanoyl)-8-O-debutanoylthapsigargin (12ADT), a potent thaspigargin (Tg) analog. Tg is a highly potent natural plant product that induces proliferation independent apoptosis in all cell types. To selectively and efficiently deliver this anti-tumoral effect to sites of prostatic cancer, prodrugs that were activated within prostate cancer by PSMA’s enzymatic activity were developed. These substrates were characterized on the basis of rates of PSMA hydrolysis and stability in human plasma. All substrates were hydrolyzed by PSMA to varying extents and stable in human plasma. Some of the synthesized 12ADT prodrugs were selectively toxic to PSMA expressing human prostate cancer cell lines. Efforts are underway to test lead therapeutic prodrugs in animal models against PSMA-producing prostate cancer xenografts. The aforementioned prodrug candidates that are especially activated by PSMA represent a novel therapy that could be given to men with prostate cancer while avoiding significant systemic toxicity.
Use of the qSOFA Score in the Emergency Department—Reply
Authors: Yonathan Freund, Ben Bloom, Bruno Riou
Journal: JAMA (2017)

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Worldwide lack of early referral of patients with alcoholic liver disease: results of the global alcoholic liver disease survey (GLADIS)
Authors: N.D. Shah, M.V. Cots, C. Zhang, N. Zahiragic, Y. Yu, M. Yacoub, P. Wu, A. Wandera, J. Vorobioff, E.S.D.S. Traquino, P.H. Thurairajah, S. Tan, S. Spreckic, E.R.A. Soler, N. Sivac, W. Siow, C. Scheurich, F. Sáez-Royuela, A. Rodil, D. Reis, S. Ono, M. Nabeshima, T.E. Kiong, M. Karoney, W. Gui, M.C. Fernández, A. Farias, C.R. Domech, P.M. Costa, M. Biryukova, A. Alfadhli, L. Yang, F. Some, R. Kochhar, J. Kluwe, W. Kim, V. Isakov, A. Husić-Selimovic, J. Hsiang, J. George, M. El Kassas, Z. Dorta, F.J. Carrilho, F. Bessone, E.B. Aranda, M. Alboraie, H. Cortez-Pinto, R. Bataller
Journal: Journal of Hepatology (2017)
Abstract IA06: Oncogenic translation programs
Authors: Hans-Guido Wendel
Journal: Cancer Research (2017)

Abstract New York, NY. I will provide an overview of the lab's contribution to deciphering the role of aberrant mRNA translation in cancer. We initially reported that aberrant eIF4E expression can drive lymphomagenesis in vivo. Next, we noticed that eIF4E's oncogenic activity strictly required phosphorylation at S209 by MNK1/2 kinases. The latter is the basis of ongoing efforts to develop and test MNK kinase inhibitors for cancer applications. More recently, we dissected the molecular basis of the anti-cancer action of eIF4A inhibitors like silvestrol. Using the ribosome footprinting technology developed by the Weissman lab we noticed that eIF4A inhibition acutely and preferentially suppressed a select group of ~200 mRNAs. These are marked by repeated 5' UTR sequences that are predicted to fold into energetically favorable G-quadruplex structures. Notably, many of these eIF4A–dependent transcripts encode oncogenic transcription factors (e.g. MYC and MYB), a number of cell cycle regulators (e.g. CDK6, CCND3), and anti-apoptotic BCL2 family genes. These findings also begin to shed light on the overarching question of how aberrant translation may lead to cancer. We speculate that it is not simply a global increase in protein production but instead the activation of oncogenic translation programs. We will discuss these findings also in light of recent work proposing an additional mechanism of eIF4A action that emphasizes binding to ubiquitous RNA sequence elements over the enzymatic activity of eIF4A. Citation Format: Hans-Guido Wendel. Oncogenic translation programs. [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 IA06.
Assessment of bile salt export pump (BSEP) inhibition by BSEP-reactive immunoglobulins from Antibody-induced BSEP deficiency patients using a novel, cell-based assay
Authors: J. Stindt, C. Dröge, M. Wammers, P. Philippski, C. Wiek, H. Hanenberg, D. Häussinger, V. Keitel
Journal: Journal of Hepatology (2017)
Abstract 15018: Is Thirst a Marker or Cause of Complicated Heart Failure Admissions?
Authors: Sunit-Preet Chaudhry, D. Marshall Brinkley, Syed Saad Mahmood, John D Groarke, Adriana Luk, Deepa M Gopal, Neal K Lakdawala, Lynne W Stevenson
Journal: Circulation (2016)

Introduction: Thirst is a source of morbidity in heart failure (HF) which may exacerbate congestion and be prognostically important. We hypothesized that patients describing increased thirst would ...
CERTAIN-1: efficacy and safety of glecaprevir/pibrentasvir in Japanese patients with chronic genotype 1 hepatitis C virus infection with and without cirrhosis
Authors: K. Chayama, F. Suzuki, Y. Karino, Y. Kawakami, K. Sato, T. Atarashi, A. Naganuma, T. Watanabe, Y. Eguchi, H. Yoshiji, M. Seike, Y. Takei, K. Kato, K. Alves, M. Burroughs, R. Redman, D.L. Pugatch, T. Pilot-Matias, W. Xie, H. Kumada
Journal: Journal of Hepatology (2017)
Phase III, randomized, double-blind, multicenter, placebo (P)-controlled trial of rilotumumab (R) plus epirubicin, cisplatin and capecitabine (ECX) as first-line therapy in patients (pts) with advanced MET-positive (pos) gastric or gastroesophageal junction (G/GEJ) cancer: RILOMET-1 study.
Authors: David Cunningham, Niall C. Tebbutt, Irina Davidenko, André M. Murad, Salah-Eddin Al-Batran, David H. Ilson, Sergei Tjulandin, Evgeny Gotovkin, Boguslawa Karaszewska, Igor Bondarenko, Mohamedtaki Abdulaziz Tejani, Anghel Adrian Udrea, Mustapha Ali Tehfe, Nigel Baker, Kelly Smith Oliner, Yilong Zhang, Tien Hoang, Roger Sidhu, Daniel Virgil Thomas Catenacci
Journal: Journal of Clinical Oncology (2015)

4000 Background: R is a fully human monoclonal antibody to hepatocyte growth factor. A phase 2 study showed improved overall survival (OS) and progression-free survival (PFS) with R + ECX vs P + ECX in MET-pos G/GEJ cancer (Lancet Oncol 2014;15:1007). This phase 3 trial evaluated the efficacy and safety of R + ECX in MET-pos G/GEJ cancer. Methods: Key eligibility criteria: ≥ 18 yr; previously untreated, pathologically confirmed unresectable advanced G/GEJ adenocarcinoma; ECOG score 0–1; tumor MET-pos by IHC; HER2-negative. Pts were randomized 1:1 to receive ECX (IV epirubicin 50 mg/m2 D1, IV cisplatin 60 mg/m2 D1, oral capecitabine 625 mg/m2BID D1−21) + R 15 mg/kg or P IV Q3W and stratified by disease extent (locally advanced vs metastatic) and ECOG score (0 vs 1). Primary endpoint: OS. A log-rank test stratified by randomization factors compared OS between arms. The study was powered to detect a HR of 0.69. Key secondary endpoints: PFS, 12-mo survival rate, objective response rate (ORR), safety and pharmacokinetics (PK). Results: 609 pts were randomized from Nov 2012 to Nov 2014. The study was stopped early based on an imbalance in deaths (R vs P: 128 vs 107 deaths, data cutoff: 27 Nov 2014). R was not superior to P for OS (one-sided test, p = 0.99). OS, PFS and ORR were statistically worse in the R arm. No subgroups seemed to benefit with R, including those with higher percentages of cells with ≥ 1+ MET expression. Most common AEs that were higher with R: peripheral edema, hypoalbuminemia, deep vein thrombosis and hypocalcemia. Conclusions: RILOMET-1 did not meet its primary endpoint; OS was statistically significantly worse with R. PK and MET biomarker analyses are pending. Clinical trial information: NCT01697072. R (n = 304) P (n = 305) R vs P Median OS,* mo 9.6 (7.9–11.4) 11.5 (9.7–13.1) HR†= 1.37 (1.06–1.78) p = 0.016 Median PFS,* mo 5.7 (5.3–5.9) 5.7 (5.5–7.1) HR†= 1.30 (1.05–1.62) p = 0.016 12-mo survival rate* 38.4% (30.2%–46.6%) 49.7% (41.5%–57.4%) Diff = -11.4 (-22.9–0.2) p = 0.053 ORR* 30% (24.6%–36.0%) 39.2% (33.3%–45.4%) Odds ratio = 0.67 (0.46–0.96) p = 0.027 *95% CI shown. †Stratified.
Thrombin Generation in Paroxysmal Nocturnal Haemoglobinuria
Authors: Audrey Krüse Zeinad, Tania RFR Rocha, Sandra Fatima Menosi Guallandro, Guilherme Henrique Hencklain Fonseca, Paula Ribeiro Villaça, Erica Okazaki, Vanderson Rocha, Elbio Antonio D'Amico
Journal: Blood (2016)
MIKIE: A randomized, double-blind, regimen-controlled, phase II, multicenter study to assess the efficacy and safety of two different vismodegib regimens in patients with multiple basal cell carcinomas.
Authors: Rainer Kunstfeld, Axel Hauschild, David Zloty, Gary Rogers, Brigitte Dreno, Lada Mitchell, Michal Starnawski, Dirk Schadendorf
Journal: Journal of Clinical Oncology (2014)

TPS9121 Background: Vismodegib, a Hedgehog signaling pathway inhibitor, is FDA and EMA approved for patients (pts) with advanced basal cell carcinoma (BCC) who are not candidates for surgery or radiotherapy. While vismodegib reduces BCC tumor burden and blocks growth of new BCCs in pts with basal cell carcinoma nevus syndrome (BCCNS), further studies are required to optimize the therapeutic index of long-term (chronic) therapy. The MIKIE study (NCT01815840) assesses the efficacy and safety of 2 intermittent vismodegib dosing regimens in pts with multiple BCCs. Methods: MIKIE is a randomized, double-blind, regimen-controlled phase II study, in adults with multiple BCCs (including BCCNS) ≥18 years with ≥1 histopathologically confirmed BCC and ≥6 clinically evident BCCs (at least three ≥5 mm in diameter). 200 pts are planned to be randomized (1:1) to regimen A or B and stratified by BCCNS status, geographic region, and immunosuppression status. In regimen A, pts receive 3 courses of vismodegib (150 mg/d) for 12 weeks followed by placebo for 8 weeks, followed by a final 12-week course of vismodegib. In regimen B, pts receive vismodegib (150 mg/d) for 24 weeks, followed by 3 alternating courses of placebo (8 weeks) followed by vismodegib (8 weeks). Total duration of treatment will be 72 weeks in both arms, with 52 weeks of follow up. Major inclusion criteria include ECOG performance status 0–2; adequate hematopoietic, hepatic, and renal function; and signed written informed consent. Major exclusion criteria include inoperable metastatic or locally advanced BCC. Primary objective includes the percentage reduction from baseline in the number of clinically evident BCCs after 72 weeks of treatment in the 2 regimens. Secondary objectives include the percentage reduction in overall size of 3 largest BCCs, the proportion of pts with a 50% reduction in BCCs, the number of pts with new BCCs, recurrence rate, and safety and tolerability (including dropout rate due to tolerability). Skindex-16 quality of life and pharmacokinetic assessments will be conducted at selected sites. The first patient was enrolled in March 2013; the study is ongoing. Clinical trial information: NCT01815840.
Abstract B03: A whole genome screening platform to identify genes that overcome the poor translation of KRAS
Authors: Jackson J. Peterson, Erin Kaltenbrun, Christopher Counter
Journal: Cancer Research (2017)

Abstract We discovered that KRAS mRNA is highly enriched in rare codons, which limited translation of the encoded KRAS protein. Accumulating evidence suggests that there is a selective pressure during tumorigenesis to overcome the poor translation of KRAS imposed by rare codons to produce more oncogenic protein and promote more malignant phenotypes. To identify how cancer cells achieve this feat, we are screening whole genome gain- and loss-of-function libraries for genes capable of increasing the translation of a rare-codon enriched fluorescent reporter. More specifically, we have created a reporter cell line encoding a rare-codon enriched GFP and a common-codon enriched mCherry protein. Normalizing to mCherry expression, we further demonstrate that FACS can effectively isolate cells expressing a common-codon enriched GFP from those expressing the rare codon counterpart. Given this, the reporter line was stably infected with a CRISPR library targeting 19,050 genes and sorted by FACS for those expressing high levels of GFP, with these cells now being subjected to deep sequencing. A whole genome ORF library is being screened in an identical fashion. In the future, we will rescreen candidate CRISPRs or ORFs identified from these screens, and those that reproducibly increase the expression of the rare-codon enriched reporter will be analyzed further, especially with regards to the underlying mechanism and expression in cancer cells. Citation Format: Jackson J. Peterson, Erin Kaltenbrun, Christopher Counter. A whole genome screening platform to identify genes that overcome the poor translation of KRAS. [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 B03.
Clonal Expansion and Long-Term Persistence of Rhesus Macaque NK Cells with an Adaptive Phenotype
Authors: Chuanfeng Wu, Diego A Espinoza, Samson J. Koelle, Di Yang, Heinrich Schlums, Jan K. Davidson-Moncada, Rong Lu, Amitinder Kaur, Hammer Quirin, Brian Li, Sandhya R. Panch, Robert E Donahue, Richard W. Childs, Chiara Romagnani, Yenan Bryceson, Cynthia E. Dunbar
Journal: Blood (2016)
Whole-genome deep sequencing of hepatitis B virus in chronic hepatitis B patients reveals single nucleotide variants associated with baseline HBV DNA levels and HBeAg status
Authors: O. Podlaha, P. Revill, N. Bhardwaj, L. Zhuo, K. Kitrinos, A. Gaggar, Z. Jiang, P. Marcellin, S. Locarnini, H.L. Chan
Journal: Journal of Hepatology (2017)
HSP27: A Therapeutic Target in Myelofibrosis
Authors: Margaux Sevin, Nicolas Pernet, Franck Vitte, Selim Ramla, Paul Sagot, Laurent Martin, Jean Luc Villeval, Catherine Lacout, Isabelle Plo, Carmen Garrido, Francois Girodon, Aurelie de Thonel
Journal: Blood (2016)
IMpower133: Phase I/III trial of first-line atezolizumab with carboplatin and etoposide in ES-SCLC
Authors: M. Reck, A.S. Mansfield, S.V. Liu, T.S.K. Mok, X. Tang, S. Lam, F. Kabbinavar, A. Lopez-Chavez, A. Sandler, L. Horn
Journal: Annals of Oncology (2017)
Soluble (s)CD163 a macrophage activation marker is associated with liver disease severity in patients with Wilson’s disease
Authors: H. Groenbaek, D.N. Gotthardt, J. Björklund, J. Pfeiffenberger, H.J. Møller, T. Bashlekova, P. Ott, K.-H. Weiss
Journal: Journal of Hepatology (2017)
Use of G-CSF and prophylactic antibiotics with concurrent chemo-radiotherapy in limited-stage small cell lung cancer: Results from the Phase III CONVERT trial
Authors: F. Gomes, C. Faivre-Finn, F. Fernandez-Gutierrez, D. Ryder, A. Bezjak, F. Cardenal, P. Fournel, J. Van Meerbeeck, F. Blackhall
Journal: Annals of Oncology (2017)
HCV eradication reduces the occurrence of major adverse cardiovascular events in hepatitis C cirrhotic patients: data from the prospective ANRS CO12 CirVir cohort
Authors: P. Cacoub, P. Nahon, R. Layese, V. Bourcier, C. Cagnot, P. Marcellin, D. Guyader, S. Pol, D. Larrey, F. Roudot-Thoraval, E. Audureau
Journal: Journal of Hepatology (2017)
Intestinal inflammation worsens epithelial barrier function in rats with cirrhosis and ascites: role of commensal gut flora
Authors: L. Muñoz, M.-J. Borrero, M. Ubeda, L. Paule, M. Lario, D. Díaz, E. Conde, M. Rodríguez-Serrano, A.-M. Sánchez-Díaz, R. del Campo, Ó. Pastor, L. García-Bermejo, M. Álvarez-Mon, A. Albillos
Journal: Journal of Hepatology (2017)
Interferon-free cure of hepatitis C virus infection does alter the soluble inflammatory milieu which could affect hepatocellular carcinoma surveillance by CD8+ T cells in patients with liver cirrhosis
Authors: S.O. Sekyere, C. Falk, A. Aregay, B. Schlevogt, K. Deterding, M.P. Manns, A. Vogel, T. Wirth, M. Cornberg, H. Wedemeyer
Journal: Journal of Hepatology (2017)
Non-invasive multiparametric MRI (LiverMultiScanTM) effectively excludes NASH and liver fibrosis in at risk patients
Authors: H.R. Wilman, M. Kelly, N. McDonald, P. Eddowes, M. Pavlides, S. Neubauer, J. Fallowfield, G. Hirschfield, R. Banerjee
Journal: Journal of Hepatology (2017)
Thymic Epithelial Tumors phenotype relies on miR-145-5p epigenetic regulation
Authors: Teresa Bellissimo, Federica Ganci, Enzo Gallo, Andrea Sacconi, Claudia Tito, Luciana De Angelis, Claudio Pulito, Silvia Masciarelli, Daniele Diso, Marco Anile, Vincenzo Petrozza, Felice Giangaspero, Edoardo Pescarmona, Francesco Facciolo, Federico Venuta, Mirella Marino, Giovanni Blandino, Francesco Fazi
Journal: Molecular Cancer (2017)

Thymoma and thymic carcinoma are the most frequent subtypes of thymic epithelial tumors (TETs). A relevant advance in TET management could derive from a deeper molecular characterization of these neoplasms. We previously identified a set of microRNA (miRNAs) differentially expressed in TETs and normal thymic tissues and among the most significantly deregulated we described the down-regulation of miR-145-5p in TET. Here we describe the mRNAs diversely regulated in TETs and analyze the correlation between these and the miRNAs previously identified, focusing in particular on miR-145-5p. Then, we examine the functional role of miR-145-5p in TETs and its epigenetic transcriptional regulation. mRNAs expression profiling of a cohort of fresh frozen TETs and normal tissues was performed by microarray analysis. MiR-145-5p role in TETs was evaluated in vitro, modulating its expression in a Thymic Carcinoma (TC1889) cell line. Epigenetic transcriptional regulation of miR-145-5p was examined by treating the TC1889 cell line with the HDAC inhibitor Valproic Acid (VPA). Starting from the identification of a 69-gene signature of miR-145-5p putative target mRNAs, whose expression was inversely correlated to that of miR-145-5p, we followed the expression of some of them in vitro upon overexpression of miR-145-5p; we observed that this resulted in the down-regulation of the target genes, impacting on TETs cancerous phenotype. We also found that VPA treatment of TC1889 cells led to miR-145-5p up-regulation and concomitant down-regulation of miR-145-5p target genes and exhibited antitumor effects, as indicated by the induction of cell cycle arrest and by the reduction of cell viability, colony forming ability and migration capability. The importance of miR-145-5p up-regulation mediated by VPA is evidenced by the fact that hampering miR-145-5p activity by a LNA inhibitor reduced the impact of VPA treatment on cell viability and colony forming ability of TET cells. Finally, we observed that VPA was also able to enhance the response of TET cells to cisplatin and erlotinib. Altogether our results suggest that the epigenetic regulation of miR-145-5p expression, as well as the modulation of its functional targets, could be relevant players in tumor progression and treatment response in TETs.
Very Rapid Production of CAR+ T-Cells upon Non-Viral Gene Transfer Using the Sleeping Beauty System
Authors: Lenka V. Hurton, Harjeet Singh, Kirsten C. Switzer, Tiejuan Mi, Leo G. Flores, Aaron Orozco, Sourindra N. Maiti, Shihuang Su, Amer Najjar, Mary Helen Huls, Partow Kebriaei, Richard E. Champlin, Laurence J.N. Cooper
Journal: Blood (2016)