tbuckley/cabot-search huggingface dataset:
EP300 Selectively Controls the Enhancer Landscape of <i>MYCN</i>-Amplified Neuroblastoma
Authors: Adam D. Durbin, Tingjian Wang, Virangika K. Wimalasena, Mark W. Zimmerman, Deyao Li, Neekesh V. Dharia, Luca Mariani, Noha A.M. Shendy, Stephanie Nance, Anand G. Patel, Ying Shao, Maya Mundada, Lily Maxham, Paul M.C. Park, Logan H. Sigua, Ken Morita, Amy Saur Conway, Amanda L. Robichaud, Antonio R. Perez-Atayde, Melissa J. Bikowitz, Taylor R. Quinn, Olaf Wiest, John Easton, Ernst Schönbrunn, Martha L. Bulyk, Brian J. Abraham, Kimberly Stegmaier, A. Thomas Look, Jun Qi
Journal: Cancer Discovery (2021)

Abstract Gene expression is regulated by promoters and enhancers marked by histone H3 lysine 27 acetylation (H3K27ac), which is established by the paralogous histone acetyltransferases (HAT) EP300 and CBP. These enzymes display overlapping regulatory roles in untransformed cells, but less characterized roles in cancer cells. We demonstrate that the majority of high-risk pediatric neuroblastoma (NB) depends on EP300, whereas CBP has a limited role. EP300 controls enhancer acetylation by interacting with TFAP2β, a transcription factor member of the lineage-defining transcriptional core regulatory circuitry (CRC) in NB. To disrupt EP300, we developed a proteolysis-targeting chimera (PROTAC) compound termed “JQAD1” that selectively targets EP300 for degradation. JQAD1 treatment causes loss of H3K27ac at CRC enhancers and rapid NB apoptosis, with limited toxicity to untransformed cells where CBP may compensate. Furthermore, JQAD1 activity is critically determined by cereblon (CRBN) expression across NB cells. Significance: EP300, but not CBP, controls oncogenic CRC-driven transcription in high-risk NB by binding TFAP2β. We developed JQAD1, a CRBN-dependent PROTAC degrader with preferential activity against EP300 and demonstrated its activity in NB. JQAD1 has limited toxicity to untransformed cells and is effective in vivo in a CRBN-dependent manner. This article is highlighted in the In This Issue feature, p. 587
Medical Debt in the US From 2009 to 2020
Authors: Nishant Uppal, Carrie Lubitz, Benjamin James
Journal: JAMA (2021)

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 HomeNew OnlineCurrent IssueFor Authors 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Evaluation of the PADIS score stratifying risk for venous thromboembolism recurrence after a first unprovoked pulmonary embolism: results from the REVERSE study
Authors: Lucia Caiano, Rhys Sharkey, Marc A. Rodger, Michael J. Kovacs, Grégoire Le Gal, Aurélien Delluc
Journal: European Respiratory Journal (2021)

Current guidelines suggest that most patients presenting with a first episode of an unprovoked venous thromboembolism (VTE) event be considered for indefinite anticoagulation, as long as their bleeding risk remains acceptably low [1, 2]. However, this exposes a considerable number of patients to long term anticoagulation as 70% of patients with a first unprovoked VTE will have no recurrence [3]. In 2010, a guidance from the International Society on Thrombosis and Haemostasis (ISTH) suggested that a 1-year cumulative rate of recurrent VTE after stopping anticoagulation of less than 5%, with a 95% confidence interval (CI) upper limit lower than 8%, is low enough to consider that long-term anticoagulant therapy would not be beneficial [4]. As such, efforts are ongoing to identify risk factors and scoring tools to help discriminate between subsets of patients whose risk/benefit ratio most- or least-strongly favours continued therapy. This study does not support that the PADIS-PE score can safely identify patients who could stop anticoagulation after a first unprovoked PE <https://bit.ly/3GOzeEl> The REVERSE investigators: P.S. Wells and T. Ramsay, Ottawa, ON, Canada; S.R. Kahn, I. Chagnon and S. Solymoss, Montreal, QC, Canada; D.A. Anderson, Halifax, NS, Canada; M. Crowther, Hamilton, ON, Canada; R. White, Sacramento, CA, USA.
Animal models for SARS‐CoV‐2 infection and pathology
Authors: Zhenfei Bi, Weiqi Hong, Jingyun Yang, Shuaiyao Lu, Xiaozhong Peng
Journal: MedComm (2021)

Abstract Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) is the etiology of coronavirus disease 2019 (COVID‐19) pandemic. Current variants including Alpha , Beta , Gamma , Delta , and Lambda increase the capacity of infection and transmission of SARS‐CoV‐2, which might disable the in‐used therapies and vaccines. The COVID‐19 has now put an enormous strain on health care system all over the world. Therefore, the development of animal models that can capture characteristics and immune responses observed in COVID‐19 patients is urgently needed. Appropriate models could accelerate the testing of therapeutic drugs and vaccines against SARS‐CoV‐2. In this review, we aim to summarize the current animal models for SARS‐CoV‐2 infection, including mice, hamsters, nonhuman primates, and ferrets, and discuss the details of transmission, pathology, and immunology induced by SARS‐CoV‐2 in these animal models. We hope this could throw light to the increased usefulness in fundamental studies of COVID‐19 and the preclinical analysis of vaccines and therapeutic agents.
The NASEM Report on Implementing High-Quality Primary Care—Implications for Pediatrics
Authors: Tumaini R. Coker, James M. Perrin
Journal: JAMA Pediatrics (2021)

This Viewpoint highlights key implications of the National Academies of Sciences, Engineering, and Medicine (NASEM) Committee on Implementing High-Quality Primary Care report for pediatric primary care as well as potential threats to its success for child health.
Glofitamab As Monotherapy and in Combination with Obinutuzumab Induces High Complete Response Rates in Patients (pts) with Multiple Relapsed or Refractory (R/R) Follicular Lymphoma (FL)
Authors: Franck Morschhauser, Carmelo Carlo-Stella, Michael Dickinson, Tycel Phillips, Roch Houot, Fritz Offner, Corinne Haioun, Paolo Corradini, Martin Hutchings, Anna Sureda, Joaquín Martínez-López, Tomasz Wrobel, Shang-Ju Wu, Linda Lundberg, Estefania Mulvihill, David Perez-Callejo, James Relf, Anesh Panchal, Kathryn Humphrey, Emmanuel Bachy
Journal: Blood (2021)
Abstract 9101: RVLM Microinjection to Explain the Role of Metabotropic Glutamate Receptors in the Regulation of Baseline Blood Pressure and Heart Rate in SHRSP
Authors: Md Zahid Hasan, Toru Nabika
Journal: Circulation (2021)

Introduction: Glutamate (Glu) is activated by the stimulation of its receptors. The microinjection of Glu in rostral ventrolateral medulla (RVLM) elicited a rapid and large increase in blood pressure (BP) and heart rate (HR), which is inhibited with kynurenic acid (KYN), a selective inhibitor of ionotropic glutamate receptors (iGluR). Further, we showed that the response to Glu was much greater in stroke-prone spontaneously hypertensive rats (SHRSP) than that in Wistar Kyoto (WKY) rats, indicating that iGluR in RVLM played an important role to maintain high BP &amp; HR in SHRSP. Whereas, the role of metabotropic glutamate receptors (mGluR) in RVLM were not fully elucidated in SHRSP yet. Hypotheses: Since the different mGluR types, e.g., group I (mGluR1, mGluR5), group II (mGluR2, mGluR3) &amp; group III (mGluR4, mGluR6, mGluR7, mGluR8), are expressed in the various regions of rat’s brain, and several studies reported that mGluR5 is largely expressed in RVLM of rats; in this study we evaluated the pathophysiological role(s) of mGluR5, expecting that mGluR5 in RVLM keeps high baseline (i) BP and (ii) HR in SHRSP. Method: MTEP (10 nmole, a highly selective mGluR5 antagonist) and KYN (4 nmole) were microinjected unilaterally in RVLM in SHRSP (n=10) and WKY (n=10) to determine the effects on baseline BP &amp; HR. In addition, the effects of two inhibitors on response to Glu (5 nmole) microinjection were observed. Results: MTEP reduced baseline BP &amp; HR significantly in SHRSP when compared to those in WKY (ΔMAP: -30±3 vs. -3±2 mmHg, ΔHR: -35±3 vs. -4±2 bpm, respectively, p&lt; 0.05), but failed to attenuate a response to Glu microinjection. In contrast, KYN had no significant effects on baseline BP &amp; HR in the two strains, whereas it showed an inhibitory effect on the response to microinjected Glu, which was significantly greater in SHRSP than that in WKY. Conclusions: This study suggested that mGluR5 in RVLM played a major role in the maintenance of high baseline BP &amp; HR in SHRSP.
Performance of a Community Based Strategy Led by Health Workers Using Lung Function Questionnaire and Pocket Spirometer for Detecting Chronic Obstructive Pulmonary Disease in Rural India
Authors: Prashant Jarhyan, Anastasia Hutchinson, R Khatkar, NS Venkateshmurthy, D Prabhakaran, S Mohan
Journal: American Journal of Respiratory and Critical Care Medicine (2018)
Nucleocapsid mutations R203K/G204R increase the infectivity, fitness, and virulence of SARS-CoV-2
Authors: Haibo Wu, Na Xing, Kaiwen Meng, Beibei Fu, Weiwei Xue, Pan Dong, Wanyan Tang, Yang Xiao, Gexin Liu, Haitao Luo, Wenzhuang Zhu, Xiaoyuan Lin, Geng Meng, Zhenglin Zhu
Journal: Cell Host & Microbe (2021)

Previous work found that the co-occurring mutations R203K/G204R on the SARS-CoV-2 nucleocapsid (N) protein are increasing in frequency among emerging variants of concern or interest. Through a combination of in silico analyses, this study demonstrates that R203K/G204R are adaptive, while large-scale phylogenetic analyses indicate that R203K/G204R associate with the emergence of the high-transmissibility SARS-CoV-2 lineage B.1.1.7. Competition experiments suggest that the 203K/204R variants possess a replication advantage over the preceding R203/G204 variants, possibly related to ribonucleocapsid (RNP) assembly. Moreover, the 203K/204R virus shows increased infectivity in human lung cells and hamsters. Accordingly, we observe a positive association between increased COVID-19 severity and sample frequency of 203K/204R. Our work suggests that the 203K/204R mutations contribute to the increased transmission and virulence of select SARS-CoV-2 variants. In addition to mutations in the spike protein, mutations in the nucleocapsid protein are important for viral spreading during the pandemic.
Single Cell RNA Sequencing Identifies Potential Molecular Indicators of Response to Melflufen in Multiple Myeloma
Authors: Philipp Sergeev, Sadiksha Adhikari, Juho J. Miettinen, Maiju-Emilia Huppunen, Minna Suvela, Ana Slipicevic, Nina N. Nupponen, Fredrik Lehmann, Caroline A. Heckman
Journal: Blood (2021)
Artificial Intelligence-Based Predictive Models for Acute Myeloid Leukemia
Authors: Ibrahim Didi, David Simoncini, Francois Vergez, Pierre-Yves Dumas, Suzanne Tavitian, Laetitia Largeaud, Audrey Bidet, Jean-Baptiste Rieu, Isabelle Luquet, Nicolas Lechevalier, Eric Delabesse, Audrey Sarry, Anne-Charlotte De Grande, Emilie Berard, Arnaud Pigneux, Christian Recher, Jean-Marc Alliot, Sarah Bertoli
Journal: Blood (2021)
Effects of fecal microbiota transplant on DNA methylation in subjects with metabolic syndrome
Authors: Eduard W. J. van der Vossen, Diogo Bastos, Daniela Stols-Gonçalves, Marcus C. de Goffau, Mark Davids, Joao P. B. Pereira, Andrew Y. F. Li Yim, Peter Henneman, Mihai G. Netea, Willem M. de Vos, Wouter de Jonge, Albert K. Groen, Max Nieuwdorp, Evgeni Levin
Journal: Gut Microbes (2021)

Accumulating evidence shows that microbes with their theater of activity residing within the human intestinal tract (i.e., the gut microbiome) influence host metabolism. Some of the strongest results come from recent fecal microbial transplant (FMT) studies that relate changes in intestinal microbiota to various markers of metabolism as well as the pathophysiology of insulin resistance. Despite these developments, there is still a limited understanding of the multitude of effects associated with FMT on the general physiology of the host, beyond changes in gut microbiome composition. We examined the effect of either allogenic (lean donor) or autologous FMTs on the gut microbiome, plasma metabolome, and epigenomic (DNA methylation) reprogramming in peripheral blood mononuclear cells in individuals with metabolic syndrome measured at baseline (pre-FMT) and after 6 weeks (post-FMT). Insulin sensitivity was determined with a stable isotope-based 2 step hyperinsulinemic clamp and multivariate machine learning methodology was used to uncover discriminative microbes, metabolites, and DNA methylation loci. A larger gut microbiota shift was associated with an allogenic than with autologous FMT. Furthemore, the data results of the the allogenic FMT group data indicates that the introduction of new species can potentially modulate the plasma metabolome and (as a result) the epigenome. Most notably, the introduction of Prevotella ASVs directly correlated with methylation of AFAP1, a gene involved in mitochondrial function, insulin sensitivity, and peripheral insulin resistance (Rd, rate of glucose disappearance). FMT was found to have notable effects on the gut microbiome but also on the host plasma metabolome and the epigenome of immune cells providing new avenues of inquiry in the context of metabolic syndrome treatment for the manipulation of host physiology to achieve improved insulin sensitivity.
A Thrombospondin-1 Release Assay (TRA) Coupled to PF4-Treated Cryopreserved Platelets for the Detection of Pathogenic HIT and VITT Antibodies
Authors: Adam Kanack, Curtis Jones, Bandana Singh, Gemlyn George, Mouhamed Yazan Abou-Ismail, David L. Green, Alison Grazioli, Rachel Leger, Nahla M. Heikal, Dong Chen, Rajiv K. Pruthi, Anand Padmanabhan
Journal: Blood (2021)
Efficacy and Safety of Umbralisib, Ublituximab (U2), and U2 Plus Bendamustine in Patients with Relapsed or Refractory Diffuse Large B-Cell Lymphoma (DLBCL)
Authors: John M. Burke, Gustavo Fonseca, Wojciech Jurczak, Jason Melear, Miguel Islas-Ohlmayer, James A Reeves, Parameswaran Venugopal, Tomasz Wróbel, Don Stevens, John M. Pagel, Jerome Goldschmidt, Hari P. Miskin, Peter Sportelli, Owen A. O'Connor, Nilanjan Ghosh
Journal: Blood (2021)
Multiyear Factor VIII Expression after AAV Gene Transfer for Hemophilia A
Authors: Lindsey A. George, Paul E. Monahan, M. Elaine Eyster, Spencer K. Sullivan, Margaret V. Ragni, Stacy E. Croteau, John E.J. Rasko, Michael Recht, Benjamin J. Samelson-Jones, Amy MacDougall, Kristen Jaworski, Robert Noble, Marla Curran, Klaudia Kuranda, Federico Mingozzi, Tiffany Chang, Kathleen Z. Reape, Xavier M. Anguela, Katherine A. High
Journal: New England Journal of Medicine (2021)

The goal of gene therapy for patients with hemophilia A is to safely impart long-term stable factor VIII expression that predictably ameliorates bleeding with the use of the lowest possible vector dose.In this phase 1-2 trial, we infused an investigational adeno-associated viral (AAV) vector (SPK-8011) for hepatocyte expression of factor VIII in 18 men with hemophilia A. Four dose cohorts were enrolled; the lowest-dose cohort received a dose of 5 × 1011 vector genomes (vg) per kilogram of body weight, and the highest-dose cohort received 2 × 1012 vg per kilogram. Some participants received glucocorticoids within 52 weeks after vector administration either to prevent or to treat a presumed AAV capsid immune response. Trial objectives included evaluation of the safety and preliminary efficacy of SPK-8011 and of the expression and durability of factor VIII.The median safety observation period was 36.6 months (range, 5.5 to 50.3). A total of 33 treatment-related adverse events occurred in 8 participants; 17 events were vector-related, including 1 serious adverse event, and 16 were glucocorticoid-related. Two participants lost all factor VIII expression because of an anti-AAV capsid cellular immune response that was not sensitive to immune suppression. In the remaining 16 participants, factor VIII expression was maintained; 12 of these participants were followed for more than 2 years, and a one-stage factor VIII assay showed no apparent decrease in factor VIII activity over time (mean [±SD] factor VIII activity, 12.9±6.9% of the normal value at 26 to 52 weeks when the participants were not receiving glucocorticoids vs. 12.0±7.1% of the normal value at >52 weeks after vector administration; 95% confidence interval [CI], -2.4 to 0.6 for the difference between matched pairs). The participants had a 91.5% reduction (95% CI, 88.8 to 94.1) in the annualized bleeding rate (median rate, 8.5 events per year [range, 0 to 43.0] before vector administration vs. 0.3 events per year [range, 0 to 6.5] after vector administration).Sustained factor VIII expression in 16 of 18 participants who received SPK-8011 permitted discontinuation of prophylaxis and a reduction in bleeding episodes. No major safety concerns were reported. (Funded by Spark Therapeutics and the National Heart, Lung, and Blood Institute; ClinicalTrials.gov numbers, NCT03003533 and NCT03432520.).
Validation of the Qualms Questionnaire to Assess Health-Related Quality of Life in European and Israeli Patients with Myelodysplastic Syndromes: Results from the MDS-Right Project
Authors: Fabio Efficace, Karin A Koinig, Francesco Cottone, David Bowen, Moshe Mittelman, Saskia M. C. Langemeijer, Dominic Culligan, Kalman Filanovsky, Gregory A. Abel, Michael Storck, Alexandra Smith, Corine Van Marrewijk, Martin Dugas, Theo M de Witte, Reinhard Stauder
Journal: Blood (2021)
PTP1B Is an Intracellular Checkpoint that Limits T-cell and CAR T-cell Antitumor Immunity
Authors: Florian Wiede, Kun-Hui Lu, Xin Du, Mara N. Zeissig, Rachel Xu, Pei Kee Goh, Chrysovalantou E. Xirouchaki, Samuel J. Hogarth, Spencer Greatorex, Kevin Sek, Roger J. Daly, Paul A. Beavis, Phillip K. Darcy, Nicholas K. Tonks, Tony Tiganis
Journal: Cancer Discovery (2021)

Abstract Immunotherapies aimed at alleviating the inhibitory constraints on T cells have revolutionized cancer management. To date, these have focused on the blockade of cell-surface checkpoints such as PD-1. Herein we identify protein tyrosine phosphatase 1B (PTP1B) as an intracellular checkpoint that is upregulated in T cells in tumors. We show that increased PTP1B limits T-cell expansion and cytotoxicity to contribute to tumor growth. T cell–specific PTP1B deletion increased STAT5 signaling, and this enhanced the antigen-induced expansion and cytotoxicity of CD8+ T cells to suppress tumor growth. The pharmacologic inhibition of PTP1B recapitulated the T cell–mediated repression of tumor growth and enhanced the response to PD-1 blockade. Furthermore, the deletion or inhibition of PTP1B enhanced the efficacy of adoptively transferred chimeric antigen receptor (CAR) T cells against solid tumors. Our findings identify PTP1B as an intracellular checkpoint whose inhibition can alleviate the inhibitory constraints on T cells and CAR T cells to combat cancer. Significance: Tumors subvert antitumor immunity by engaging checkpoints that promote T-cell exhaustion. Here we identify PTP1B as an intracellular checkpoint and therapeutic target. We show that PTP1B is upregulated in intratumoral T cells and that its deletion or inhibition enhances T-cell antitumor activity and increases CAR T-cell effectiveness against solid tumors. This article is highlighted in the In This Issue feature, p. 587
316 Leucine-rich repeats and immunoglobulin-like domains protein 1 is highly expressed on tumor-infiltrating T cells and may play a role in modulating T cell activation
Authors: Li Wang, Timothy Chan, Cassandra Gilmour, Keman Zhang, Tyler Alban, Hieu Ta, Hieu Ta
Journal: Journal for ImmunoTherapy of Cancer (2021)

Background Immune checkpoint receptors (ICRs) regulate T cell-mediated immune responses to self - and neo-antigens, thereby play an important role in the development of autoimmunity and immune responses to infections. In cancer, ICRs such as PD-1 and CTLA4 impair immuno-surveillance against neoplastic cells, while other costimulatory molecules like ICOS, OX40 could augment the immune responses. Immunotherapy that targets either inhibitory or costimulatory immune checkpoint have become the breakthrough therapy for cancer treatment. However, the efficacy of this class of therapy is limited to a fraction of patients, pointing the need to overcome non-redundant immuno-inhibitory pathways or discover new immuno-costimulatory pathways. Methods Examining surface proteins that are highly expressed in various mouse tumors by flow cytometry and immuno-histochemistry Results This study identified the expression of Leucine-rich repeats and immunoglobulin-like domains protein 1 (LRIG1) in activated CD4+ and CD8+ T cells. LRIG1 is a type-I transmembrane protein with 1092 amino acids (120 kD) and ubiquitous tissue expression patterns. We show that LRIG1 expression is not detectable on naïve CD4+ and CD8+ murine T cells but is induced upon T cell receptor (TCR) stimulation in vitro, and in tumor-infiltrating lymphocytes (TILs) from multiple murine models. We also detected LRIG1 expression on CD4+ and CD8+ TILs in several types of cancer patients such as non-small-cell lung cancer, breast cancer, melanoma, B cell lymphoma. Conclusions LRIG1 was originally identified as a tumor suppressor gene in a variety of tissues, but its expression and function have not been explored in immune cells. Our data suggest that LRIG1 is highly expressed in TILs in multiple cancer types and might play a role in regulating the anti-tumor immune response Ethics Approval Our studies have been approved by the ethics committee of the Cleveland Clinic. Consent Written informed consent was obtained from the patient for publication of this abstract and any accompanying images. A copy of the written consent is available for review by the Editor of this journal.
High-Dose Methotrexate Is Not Associated with Reduction in CNS Relapse in Patients with Aggressive B-Cell Lymphoma: An International Retrospective Study of 2300 High-Risk Patients
Authors: Katharine Louise Lewis, Lasse H. Jakobsen, Diego Villa, Sabela Bobillo, Karin Ekstroem Smedby, Kerry J. Savage, Toby A. Eyre, Kate Cwynarski, Paris L Caporn, Joan Van Zyl, Magdalena Klanova, Marek Trněný, Robert Puckrin, Douglas A. Stewart, Mark J Bishton, Christopher P. Fox, Aung M Tun, Gita Thanarajasingam, Faouzi Djebbari, Erel Joffe, Sandra Eloranta, Sara Harrysson, Laurie H. Sehn, Seth M Maliske, Kittika Poonsombudlert, Xiao Guo, Greg Hapgood, Kate Manos, Eliza Hawkes, Jahanzaib Khwaja, Adrian Minson, Michael Dickinson, Andreas Kiesbye Øvlisen, Gareth P Gregory, Michael Gilbertson, Isaac T Streit, Hamish W Scott, Matthew Ku, Sanjay de Mel, Kar Ying Yong, Liu Xin, Mridula Mokoonlall, Dipti Talaulikar, Nicholas L McVilly, Anna Johnston, Matthew J Brunner, Priyanka A Pophali, Matthew J. Maurer, Tarec Christoffer El-Galaly, Chan Yoon Cheah
Journal: Blood (2021)
Characteristics and Outcome of Elderly Patients (&amp;gt; 55 Years) with Acute Lymphoblastic Leukemia (ALL)
Authors: Daniela V. Wenge, Klaus Wethmar, Corinna Klar, Hedwig Kolve, Tim Sauer, Linus Angenendt, Georg Evers, Simon Call, Andrea Kerkhoff, Cyrus Khandanpour, Torsten Kessler, Rolf M. Mesters, Christoph Schliemann, Jan-Henrik Mikesch, Christian Reicherts, Monika Brüggemann, Wolfgang E. Berdel, Georg Lenz, Matthias Stelljes
Journal: Blood (2021)