tbuckley/cabot-search huggingface dataset:
Food allergy and omics
Authors: Gopal Krishna Dhondalay, Efren Rael, Swati Acharya, Wenming Zhang, Vanitha Sampath, Stephen J. Galli, Robert Tibshirani, Scott D. Boyd, Holden Maecker, Kari Christine Nadeau, Sandra Andorf
Journal: Journal of Allergy and Clinical Immunology (2018)
Erratum: Corrigendum: A new class of highly potent, broadly neutralizing antibodies isolated from viremic patients infected with dengue virus
Authors: Wanwisa Dejnirattisai, Wiyada Wongwiwat, Sunpetchuda Supasa, Xiaokang Zhang, Xinghong Dai, Alexander Rouvinsky, Amonrat Jumnainsong, Carolyn Edwards, Nguyen Than Ha Quyen, Thaneeya Duangchinda, Jonathan M Grimes, Wen-Yang Tsai, Chih-Yun Lai, Wei-Kung Wang, Prida Malasit, Jeremy Farrar, Cameron P Simmons, Z Hong Zhou, Felix A Rey, Juthathip Mongkolsapaya, Gavin R Screaton
Journal: Nature Immunology (2015)
What Exactly Is an “SNF-ist?”
Authors: Suzanne M. Gillespie, Cari R. Levy, Paul R. Katz
Journal: JAMA Internal Medicine (2018)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Internal Medicine journal
Long-Term Follow-up ZUMA-1: A Pivotal Trial of Axicabtagene Ciloleucel (Axi-Cel; KTE-C19) in Patients with Refractory Aggressive Non-Hodgkin Lymphoma (NHL)
Authors: Sattva S. Neelapu, Frederick L. Locke, Nancy L. Bartlett, Lazaros J. Lekakis, David B. Miklos, Eric D. Jacobsen, Ira Braunschweig, Olalekan O. Oluwole, Tanya Siddiqi, Yi Lin, John M Timmerman, Patrick M. Reagan, Adrian Bot, John M. Rossi, Lynn Navale, Yizhou Jiang, Jeff S. Aycock, Meg Elias, Jeffrey S. Wiezorek, William Y. Go
Journal: Blood (2017)
COnsensus statement on mandatory measurements in PAncreatic cancer trials for systemic treatment of unresectable disease (COMM-PACT)
Authors: L.B. van Rijssen, E. ter Veer, M.G. Besselink, R.M.A. Mali, J. Berlin, S. Boeck, F. Bonnetain, T. Conroy, G. Deplanque, D. Goldstein, B. Glimelius, J.P. Neoptolemos, M. Reni, W. Scheithauer, J. van der Meer, J.W. Wilmink, M.J. van der Poel, O.R. Busch, M.G.H. van Oijen, H.W.M. van Laarhoven
Journal: Annals of Oncology (2017)
Human poliovirus receptor CD155 enhances the proliferation of Ras gene-mutant cells.
Authors: Tokuyuki Kono, Yasuo Imai, Shin-ichi Yasuda, Yoshikazu Kuroda, Takahiro Fujimori
Journal: Cancer Research (2007)

2811   Human poliovirus receptor CD155 serves as an entry receptor for poliovirus in human and is a member of immunoglobulin superfamily. CD155 is also the homolog of Nectin-like molecule-5 (Necl-5), which works as an adhesion molecule of the cells in mice. CD155 was shown to be  overexpressed in many human cancer cells, but its roles and significance are not clear. Recently, it was reported that Necl-5 enhances cell proliferation by enhancement of Serum- and Platelet-derived Growth Factor through the Ras-Raf-MEK-ERK signaling.  We investigated the function of CD155 about the cell proliferation and its signaling pathways to elucidate the role of CD155 in the cells. The  CD155  cDNA or  CD155-  Δ  CP  cDNA (cytoplasmic deletion mutant of CD155 which works as a dominant negative of CD155) inserted in pCAGIPuro plasmids were induced to NIH3T3 (mouse fibroblast) cells, V12Ras-NIH3T3 (mouse fibroblast cells transfected with  ras  mutant gene) cells, and DLD-1 (human colon cancer) cells, respectively, establishing the cells stably expressing CD155 or CD155-ΔCP. The cells transfected only with pCAGIPuro plasmids were also established as control cells. The serum sensitivity to cell proliferation and cell growth were examined by counting the cells with Coulter Counter after 4-day incubation in DMEM supplemented with each density of FBS and after each days incubated with 7% FBS in DMEM. And the phases of the cell cycle were also examined by using fluorescence-activated cell sorter (FACS) after stimulation with 7% FBS in DMEM for 9 or 16 hours. Compared with control cells, the serum sensitivity and cell growth rate of NIH3T3/CD155 cells were decreased, but those of V12Ras-NIH3T3/CD155 cells were increased. And the serum sensitivity of V12Ras-NIH3T3/CD155-ΔCP cells was less enhanced compared with that of V12Ras-NIH3T3/CD155 cells. No significant change of serum sensitivity of DLD-1/CD155 cells, endogenously expressing CD155 and having K- ras  gene-mutation, was seen compared with that of control cells. But in DLD-1/CD155-ΔCP cells, the serum sensitivity was decreased compared with those of control cells and DLD-1/CD155-ΔCP cells. This is assumed to be due to inhibition of endogenous CD155 by CD155-ΔCP. In FACS analysis, the shortening of the period of G0/G1 phase was seen in V12Ras-NIH3T3/CD155 cells compared with that of control cells.  These results indicate that CD155 enhances the cell proliferation by shortening the period of G0/G1 phase in  Ras  gene-mutant cells.
Abstract 16: A Minipig Genetic Model of Hypertrophic Cardiomyopathy
Authors: Eric M Green, Robert M Weiss, Abhay Divekar, Sadie R Bartholomew Ingle, Marcus Henze, Raja Kawas, Lindsey Gifford, Melissa K Davis, Frank Rohret, Daniel R Thedens, Hector M Rodriguez, Marc J Evanchik, Robert L Anderson, Jessica Sieren, Christopher S Rogers, David K Meyerholz, Ferhaan Ahmad
Journal: Circulation Research (2017)

Introduction: Hypertrophic cardiomyopathy (HCM) is a heritable disease of heart muscle associated with increased risk of heart failure and sudden death. Mutations in genes encoding sarcomere proteins are commonly associated with HCM. However, the mechanisms by which these mutations lead to molecular, cellular and organ-level pathophysiology are uncertain, partly because of the lack of model systems amenable to integrated translational studies. Methods: Using homologous recombination and somatic cell nuclear transfer, we generated Yucatan minipigs with a heterozygous knock-in of the R403Q mutation in MYH7 , a well-characterized human HCM mutation. We conducted deep phenotyping with biomechanical studies of myocardial tissue samples, circulating biomarker analysis, cardiac imaging and histologic and multi-omic analysis of LV biopsy samples. Results: We followed a cohort of 22 R403Q pigs and 6 WT herdmates. Juvenile animals (3 months) showed early signs of HCM with elevated serum troponin I, increased myocardial contractility in muscle fibers and hearts and interstitial fibrosis and myocyte disarray. At late adolescence (9 months), disarray and fibrosis had progressed, but contractility had normalized with some pigs progressing to systolic dysfunction. Across the cohort, end-diastolic pressure was increased with evidence of diastolic dysfunction and elevation in B-type natriuretic peptide. Transcriptomic analysis at both 3 and 9 months showed dysregulation of metabolic modules and an upregulation of pro-fibrotic pathways. By one year of age, 11 of 22 R403Q pigs had suffered sudden cardiac death, whereas all wildtype pigs survived. Conclusions: We have developed the first large-animal genetic model of HCM. Young pigs with the MYH7 R403Q mutation show functional and histologic features of the preclinical human phenotype, and late adolescent animals have signs of advanced disease with an increased rate of sudden cardiac death. These data suggest that our minipig model may yield insights throughout the natural history of HCM from preclinical to end-stage disease. This model will thus be invaluable for advancing understanding of HCM and for the development of novel therapeutics.
Abstract 17889: Angiotensin-Neprelysin Inhibition is Superior to ACE Inhibition in Advanced Chronic Heart Failure
Authors: Gregor Poglajen, Martina Jaklic, Vesna Androcec, Gregor Zemljic, Sabina Frljak, Andra Cerar, Renata Okrajek, Miran ebetjen, Bojan Vrtovec
Journal: Circulation (2016)

Introduction:  Although angiotensin-neprilysin inhibition (ARNI) was shown to be superior to ACE inhibition (ACEI) in general heart failure population, data on patients with advanced chronic heart failure are lacking.   Hypothesis:  We sought to evaluate the safety and efficacy of ARNI in patients with advanced chronic heart failure.   Methods:  In a prospective single-center randomised study 55 patients with advanced chronic heart failure (NYHA III) were randomly allocated in a 1:1 ratio to continue with the optimal medical therapy (ACEI group) or to recieve ARNI instead or ACE (ARNI group). Patients were followed for 3 months; blood biochemical analysis, transthoracic echocardiography and ergospirometry were performed at baseline and at the end of follow-up.   Results:  At baseline ARNI group (N=28) and ACEI group (N=27) did not differ significantly regarding gender (male 70% in ARNI group vs. 77% in ACEI group;P=0.54), age (55 years vs. 56 years;P=0.67), heart failure etiology (ischemic 45% vs. 35%;P=0.41), diabetes (26% vs. 15%;P=0.32), serum potassium (4.8±0.3 mmol/L vs. 4.6±0.7 mmol/L;P=0.19), creatinine (89±28 μmol/L vs. 98±23 μmol/L;P=0.20), NT-proBNP (2335±1983 pg/mL vs. 2897±1907 pg/mL), left ventricular ejection fraction (LVEF) (26±5% vs. 25±7%;P=0.63) and exercise capacity as measured by VO2max (15.7±2.7 mL/kg/min vs. 14.3±3.7 mL/kg/min). At 3 months ARNI group in comparisson to ACEI group displayed significantly improved LVEF (32±6% vs. 27±8%;P=0.02), NT-pro-BNP (1542±1591 pg/mL vs. 2833±1724 pg/mL;P=0.01) and showed a trend to improved exercise capacity (17.3±1.8 mL/kg/min vs. 14.6±2.6 mL/kg/min;P=0.10). Similar rates of symptomatic hypotension (11% vs. 15%;P=0.69) were observed in both groups and no inter-group differences were found regarding serum potassium (4.8±0.4 mmol/L vs. 4.7±0.6 mmol/L;P=0.65).   Conclusions:  ARNI appears to be safe and efficient in patients with advanced chronic heart failure. Larger trials are needed to confirm these preliminary data and to establish potential survival benefit of ARNI in this patient cohort.
Visualization of the therapeutic efficacy of a gene correction approach in Wilson’s disease by laser-ablation inductively coupled mass spectrometry
Authors: Daniel Moreno, Oihana Murillo, Cristina Gazquez, Ruben Hernandez-Alcoceba, Ricarda Uerlings, Gloria Gonzalez-Aseguinolaza, Ralf Weiskirchen
Journal: Journal of Hepatology (2018)
Prognosis significance of HER2/neu overexpression and amplification in patients with curatively resected gastric cancer.
Authors: Fei Zhou, Ning Li, Zhaolai Hua, Lin Xia, Liwei Wang
Journal: Journal of Clinical Oncology (2012)

e14539 Background: HER-2/neu targeted therapy has been successfully used in advanced gastric cancer, but the role of HER-2/neu inprognosis of gastric cancer is not yet clear. To investigate the correlation between HER-2/neu expression and amplification and their associations with clinicopathologic outcomes and prognosis in patients with curatively resected gastric cancer. Methods: We constructed tissue microarray blocks containing &gt;70% of gastric cancer tissue and matched adjacent normal gastric tissue for 229 patients. Expression of the HER-2/neu protein in these specimens was analyzed using immunohistochemical (IHC) staining. Amplification of HER-2/neu was also analyzed for the same samples using fluorescence in situ hybridization (FISH). Kaplan Myers curve and Cox proportional hazards model were used to assess the survival. Results: Of the 229 gastric cancer samples, 14.85% were positive for HER-2/neu protein expression that was closely correlated to the Lauren type, degree of differentiation, tumor size, lymph node metastasis and overall survival. Overall, 11.79% of the 229 gastric cancers were positive for amplification of HER-2/neu, which was also closely correlated to the Lauren type, degree of differentiation, tumor size and overall survival. Moreover, Cox proportional hazards model showed that positive expression of HER-2/neu, Lauren type, tumor size, vessel invasion, TNM stage were independent prognostic factor. Both IHC and FISH assays provide an important prognostic factor for gastric cancer with a concordance rate of 96.9%, but IHC was a stronger independent prognostic factor. Conclusions: Expression of the HER-2/neu protein, compared with its gene amplification, was an independent and more sensitive prognostic factor for curatively resected gastric cancer patients.
Prognostic value of psychosocial factors for first and recurrent hospitalizations and mortality in heart failure patients: insights from the OPERA‐HF study
Authors: Ioanna Sokoreli, Steffen C. Pauws, Ewout W. Steyerberg, Gert‐Jan de Vries, Jarno M. Riistama, Aleksandra Tesanovic, Syed Kazmi, Pierpaolo Pellicori, John G. Cleland, Andrew L. Clark
Journal: European Journal of Heart Failure (2018)
Efficacy, safety, and tolerability of dolutegravir-rilpivirine for the maintenance of virological suppression in adults with HIV-1: phase 3, randomised, non-inferiority SWORD-1 and SWORD-2 studies
Authors: Josep M Llibre, Chien-Ching Hung, Cynthia Brinson, Francesco Castelli, Pierre-Marie Girard, Lesley P Kahl, Elizabeth A Blair, Kostas Angelis, Brian Wynne, Kati Vandermeulen, Mark Underwood, Kim Smith, Martin Gartland, Michael Aboud
Journal: The Lancet (2018)
Abstract 15786: Effect of Inorganic Nitrate on Wave Reflections vs. Microvascular Dilatory Reserve: Role in Improving Aeobic Capacity in Heart Failure With Preserved Ejection Fraction
Authors: Julio A Chirinos, Melissa Beraun, Raymond R Townsend, Swapna Varakantam, Payman Zamani
Journal: Circulation (2016)

Background: We have previously shown that a single dose of Inorganic nitrate supplementation increases peak oxygen consumption in heart failure with preserved ejection fraction (HFpEF). Inorganic n...
Abstract 18617: Effect of Dietary Fibre Intake and the Gut Microbiota in a Model of Heart Failure
Authors: Francine Marques, Erin Nelson, Po-Yin Chu, Duncan Horlock, April Fiedler, Mark Ziemann, Jian Tang, Sanjaya Kuruppu, Niwanthi Rajapakse, Alsam El-Osta, Charles Mackay, David Kaye
Journal: Circulation (2016)

Introduction: Although dietary intake of fruit and vegetables is associated with lower incidence of cardiovascular disease, the mechanism involved is not clear. Consumption of a diet high in fibre ...
An Antimicrobial Peptide and Its Neuronal Receptor Regulate Dendrite Degeneration in Aging and Infection
Authors: Lezi E, Ting Zhou, Sehwon Koh, Marian Chuang, Ruchira Sharma, Nathalie Pujol, Andrew D. Chisholm, Cagla Eroglu, Hiroaki Matsunami, Dong Yan
Journal: Neuron (2018)
Protein phosphatase 2A interacts with Chk2 and regulates its phosphorylation at thr-68 after cisplatin treatment of human ovarian cancer cells
Authors: Xiaobing Liang, Jing Jie Yu, Eddie Reed
Journal: Cancer Research (2005)

5560   High-fidelity maintenance of genomic integrity in eukaryotes is ensured by cell cycle checkpoints and DNA repair. The checkpoint kinase Chk2 has been implicated in both of these responses. In response to DNA damage, Chk2 is initially phosphorylated at Thr-68, which leads to its full activation. The fully activated Chk2 then phosphorylates downstream substrates of cell cycle control. However, the mechanism of inactivation of Chk2 remained unknown. PP2A plays an essential role in cell cycle regulation and induction of G 2  arrest by a mechanism of phosphorylation / dephosphorylation with a variety of protein kinases. Is Chk2 inactivated by PP2A? Do Chk2 and PP2A directly interact in DNA damage-repair signaling? Data from our investigation provide evidence that PP2A associates with Chk2 as a complex in cells and functions as a negative regulator of Chk2 signaling by dephosphorylating p-Chk2. Our findings demonstrate: i) Chk2 and PP2A are co-localized in cells, and the holoenzyme of PP2A (subunits A, B and C) co-immunoprecipatates with p-Chk2; ii) inhibition of PP2A by okadaic acid, an inhibitor of PP2A, and by siRNA to PP2A, resulted in enhanced Chk2 phosphorylation, implicating a direct enzyme-substrate relationship; iii) adenosine 3’, 5’-cyclic monophosphate (cAMP) mediated PP2A inhibition, and enhanced Chk2 phosphorylation; and iv) an  in vitro  PP2A dephosphorylation assay shows that PP2A dephosphorylates p-Chk2. These findings reveal a mechanism of intracellular signaling whereby the protein serine/threonine kinase Chk2 is regulated by a tightly associated protein serine/threonine phosphatase PP2A.
DISCREPANCIES IN ASSESSING HBV REPLICATION BY SERUM HBeAg AND HBV- DNA. THEIR RELATION TO HDV INFECTION
Authors: E Sagnelli, Fm Felaco, P Filippini, P. Pontisso, A Alberti, P Peinetti, E Buonaugurio, L Aprea, F Piccinino, G. Giusti
Journal: Journal of Hepatology (1987)
Impact of Kras Codon Sub-types In A Phase Ii Second-line Trial In Kras-mutant Advanced Non-small Cell Lung Cancer (nsclc) of Selumetinib Plus Docetaxel Versus Docetaxel Alone
Authors: T Liptrot, H Mann, I Smith, G Mcwalter, B Dougherty, J Walker, Mc Orr, D Hodgson, At Shaw, Pereira, G Jeannin, J Vansteenkiste, Che Barrios, Fa Franke, L Crinò, Pa Janne, P. Smith
Journal: Journal of Thoracic Oncology (2013)
Potassium intake modulates the thiazide-sensitive sodium-chloride cotransporter (NCC) activity via the Kir4.1 potassium channel
Authors: Ming-Xiao Wang, Catherina A. Cuevas, Xiao-Tong Su, Peng Wu, Zhong-Xiuzi Gao, Dao-Hong Lin, James A. McCormick, Chao-Ling Yang, Wen-Hui Wang, David H. Ellison
Journal: Kidney International (2018)
Transcoronary concentration gradients of circulating microRNAs in heart failure
Authors: Salvatore De Rosa, Francesca Eposito, Cristina Carella, Antonio Strangio, Giuseppe Ammirati, Jolanda Sabatino, Fabio Giovanni Abbate, Claudio Iaconetti, Vincenzo Liguori, Valerio Pergola, Alberto Polimeni, Silvio Coletta, Clarice Gareri, Bruno Trimarco, Giuseppe Stabile, Antonio Curcio, Ciro Indolfi, Antonio Rapacciuolo
Journal: European Journal of Heart Failure (2018)
A phase I trial of selective PI3K inhibitor taselisib (tas) plus palbociclib (palb) with and without endocrine therapy incorporating pharmacodynamic (PD) studies in patients (pts) with advanced cancers.
Authors: Joline Si Jing Lim, Uzma Saddia Asghar, Nikolaos Diamantis, Sarah Emily Ward, Mona Parmar, Beth Purchase, Florence I. Raynaud, Karen E Swales, Sarah Hrebien, Emma Hall, Holly Tovey, Hannah Bye, Paula Proszek, Juanita Suzanne Lopez, Alison Joanne Turner, Johann S. De Bono, Udai Banerji, Timothy Anthony Yap, Nicholas C. Turner
Journal: Journal of Clinical Oncology (2017)

2573 Background: The phosphatidylinositol 3-kinase (PI3K) pathway is commonly mutated in cancer. Tas is a selective β-isoform-sparing PI3K inhibitor with improved therapeutic index compared to pan-PI3K inhibitors. Palb is a CDK4/6 inhibitor now standard of care in combination with endocrine therapy (ET) in hormone receptor positive breast cancer. Combination of Tas, Palb and ET is synergistic in preclinical models. Methods: This investigator-initiated study investigated safety and tolerability, pharmacokinetics (PK), PD and antitumor activity of Tas+Palb, with addition of ET in dose expansion. Pts were enrolled in 3+3 dose escalation design. Tas was given continuously or 3-weeks-on, 1-week-off (3/1), Palb was given on 3/1 schedule. PD studies included analyses of platelet-rich plasma (PRP) (n = 20) and paired tumor biopsies (n = 5). Serial circulating tumor DNA was monitored in pts with PIK3CA mutations. Results: 24 pts were treated, 22 with Tas+Palb, 2 with Tas+Palb+fulvestrant(ful); M/F 11/13, median lines prior therapy 4. Treatment was well tolerated with mainly G1-2 toxicities. Most frequent G3 toxicities were neutropenia (5/24), thrombocytopenia (5/24) and rash (5/24), with no G4/5 toxicities. Two pts had dose-limiting toxicities (DLT) at DL2. No DLTs were observed at DL4, although pts experienced delayed neutrophil recovery. PK was linear and comparable with monotherapy. At 125mg Palb, significant decreases in pAKT and pGSK3β in PRP confirmed PI3K target inhibition. Two pts with PI3KCA H1047R mutant breast cancers have ongoing RECIST partial response; 1 pt with PIK3CA E542K colorectal cancer had stable disease for 20 weeks. Conclusions: Tas+Palb is well tolerated with evidence of PD and antitumor activity. Dose expansion including recruitment to triplet Tas+Palb+ful and Tas+Palb+letrozole is ongoing with continuous Tas 2mg QD, and Palb 100mg QD on 3/1 schedule, increasing to 125mg after cycle 1 in absence of myelosuppression. Clinical trial information: NCT02389842. [Table: see text]
Clinical Significance of PD-1 and PD-L1 Expression and Ongoing Interaction in the Tumor Microenvironment in Diffuse Large B Cell Lymphoma (DLBCL) Treated with R-CHOP
Authors: Zijun Yidan Xu-Monette, Li Yu, Thai Tran, Lisa Adams, Nathan Roscoe, Ganiraju Manyam, Carlo Visco, Alexandar Tzankov, Karen Dybkær, Govind Bhagat, April Chiu, Wayne Tam, Youli Zu, Eric D. Hsi, Joannes H.J.M. Van Krieken, Jooryung Huh, Maurilio Ponzoni, Andres Ferreri, Michael Boe Møller, Miguel Angel Piris, Jane N. Winter, L. Jeffrey Medeiros, George Rassidakis, Christine Angela Vaupel, Yong Li, Naveen Dakappagari, Ken H. Young
Journal: Blood (2017)
Whom to Treat for High Blood Pressure—Time for a Precision Approach
Authors: Andrew E. Moran, Mark J. Pletcher, Kirsten Bibbins-Domingo
Journal: JAMA Internal Medicine (2018)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Internal Medicine journal
Autologous T Cells Modified to Co-Express CD33-Specific Chimeric Antigen Receptor and a Kill Switch for Treatment of CD33+ Acute Myeloid Leukemia
Authors: Degang Song, Michael H Swartz, Linhua Tian, Fernando Carvajal-Borda, Jacques Plummer, Rutul R Shah, William G Wierda, Laurence J N Cooper, Tim Chan
Journal: Blood (2017)
Abnormal Karyotype and Prognosis in Polycythemia Vera: A Single Center Experience in 239 Informative Cases
Authors: Sonia Cerquozzi, Daniela Barraco, Curtis A. Hanson, Rhett P. Ketterling, Animesh Pardanani, Naseema Gangat, Ayalew Tefferi
Journal: Blood (2016)
Heavy Consumption of Alcohol is Not Associated With Worse Outcomes in Patients With Idiosyncratic Drug-induced Liver Injury Compared to Non-Drinkers
Authors: Lara Dakhoul, Marwan Ghabril, Jiezhun Gu, Victor Navarro, Naga Chalasani, Jose Serrano
Journal: Clinical Gastroenterology and Hepatology (2018)