tbuckley/cabot-search huggingface dataset:
Abstract MP135: Cardiac Sarcoplasmic Reticulum Calcium Cycling is Regulated by Kinase Independent Function of Pi3kgamma
Authors: Maradumane L Mohan, Conner P Witherow, Robert S Papay, Sathyamangla V Naga Prasad
Journal: Circulation Research (2020)

Genetic deletion of Phosphoinositide 3-kinase (PI3Kγ) in mice (PI3Kγ -/- ) results in increased cAMP levels and enhanced ventricular contractility. We investigated whether the lack of PI3Kγ plays a role in cardiac contractility by altering intracellular calcium recycling. Isolated cardiomyocytes from PI3Kγ -/- mice showed significantly reduced calcium reuptake by sarcoendoplasmic reticulum (SR) following caffeine induced calcium release indicating that PI3Kγ locally regulates the function of SR. The intracellular calcium remained at elevated levels in the cardiomyocytes of PI3Kγ -/- for a prolonged period after caffeine treatment. This could be due to changes in phosphorylation of SERCA2, Ryanodine receptor (RyR 2 ) or phospholamban (PLN). In fact, when we looked at phosphorylation of PLN in cardiac lysates, a major regulator of cardiac contractility and relaxation, PI3Kγ -/- mice showed significantly reduced PLN phosphorylation compared to littermate controls. Previous studies from our laboratory suggested that absence of PI3Kγ leads to increase in protein phosphatase (PP) activity which could be possible reason for rapid dephosphorylation of PLN, resulting in inhibition of SERCA2 pump. We observed increased SR associated PP activity and PLN associated PP activity in PI3Kγ -/- mice. We also observed increased association of PP-1 and PP2A with PLN in the absence of PI3Kγ. The altered calcium handling in the cardiomyocytes of PI3Kγ -/- mice could be restored to the level of WT controls by okadaic acid mediated inhibition of PP, suggesting that PI3Kγ plays a role in regulating PP activity associated with SR. To test whether PI3Kγ activity is required for PLN dephosphorylation and SR calcium cycling, we used mice with cardiac specific overexpression of kinase dead PI3Kγ (PI3Kγ inact ) in global PI3Kγ -/- mice (PI3Kγ inact /PI3Kγ -/- ). PI3Kγ inact /PI3Kγ -/- mice showed restored PLN phosphorylation, improved caffeine induced calcium reuptake, decreased SR and PLN associated PP activity. These studies show a novel regulation of PP and SR calcium regulation by kinase independent function of PI3Kγ. The underlying mechanism of PP regulation by PI3Kγ will be presented.
Impact of Etiological Cytogenetic Abnormalities on Immunoparesis and Progression-Free and Overall Survival in Newly Diagnosed Multiple Myeloma
Authors: Jessica Caro, David Cairns, Tom Menzies, Charlotte Pawlyn, Eileen M Boyle, Gareth Morgan, Gordon Cook, Martin F. Kaiser, Roger G Owen, Walter M Gregory, Graham H Jackson, Brian Walker, Jennifer LJ Heaney, Mark T Drayson, Faith E. Davies
Journal: Blood (2020)
ZNF410 Uniquely Activates the NuRD Component CHD4 to Silence Fetal Hemoglobin Expression
Authors: Xianjiang Lan, Ren Ren, Ruopeng Feng, Lana C Ly, Yemin Lan, Zhe Zhang, Nicholas Aboreden, Kunhua Qin, John R Horton, Jeremy D. Grevet, Thiyagaraj Mayuranathan, Osheiza Abdulmalik, Cheryl A. Keller, Belinda Giardine, Ross C. Hardison, Merlin Crossley, Mitchell J. Weiss, Xiaodong Cheng, Junwei Shi, Gerd A. Blobel
Journal: Blood (2020)
Single Agent CD45-Targeted Antibody Drug Conjugate Enables Full Mismatch Allogeneic Hematopoietic Stem Cell Transplantation in a Murine HSCT Model
Authors: Sharon L. Hyzy, Jennifer L Proctor, Geoff O Gillard, Katelyn J. Hammond, Ganapathy N. Sarma, Asim Saha, Nicholas Clark, Anjali Bhat, Tahirih L Lamothe, Rahul Palchaudhuri, Bradley R Pearse, Charlotte F McDonagh, Hans-Peter Kiem, John E Wagner, Bruce R. Blazar, Anthony E Boitano, Michael P Cooke, John C. Davis
Journal: Blood (2020)
THU0077 Interations between inflammatory polyarthritis and cardiovascular disease
Authors: PH Dessein, AE Stanwix, BI Joffe, EA Shipton
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> Inflammatory polyarthritis (IP) and cardiovascular disease (CVD) may share a common predisposition and disease activity in IP may be complicated by worsening of CVD risk factors profiles. <h3>Objectives</h3> The aim of the present study was to provide evidence for these hypotheses. <h3>Methods</h3> A literature search on predisposing factors for IP and a case controlled study in 87 IP patients (38 rheumatoid arthritis, 29 spondyloarthropathy and 20 undifferentiated inflammatory arthritis) on CVD risk factors were performed. <h3>Results</h3> Recently identified predisposing factors for IP bear remarkable similarities to CVD risk factors. They include ageing, obesity, smoking, elevated cholesterol and apolipoprotein (apo) (a) concentrations, subtle hypoadrenalism, decreased unsaturated fat intake and antioxidant concentrations, no alcohol intake, infections and stressful life events. Indeed, activation of nuclear factor kappa B, monoclonal expansion of proinflammatory CD4<sup>+</sup>CD28- T cells and acute phase responses (APR), the mutually reinforcing relationship between obesity/insulin resistance (IR) and hypoadrenalism and, endothelial dysfunction may each play a pivotal role in both IP and CVD. In established IP, disease activity associates with the presence of APR, raised apo (a), cholesterol/HDL-cholesterol and apo B/A1 ratios, IR and decreased dehydroepiandrosterone sulphate (DHEAS) concentrations, thereby worsening CVD risk factor profiles. Three studies reported a 60–80% excess CVD mortality in rheumatoid arthritis. In a more recent investigation, in which disease modifying agents were instituted soon after disease onset, the 10 year survival was similar to the general population. In our controlled study, IP was associated with a positive family history for coronary artery disease (p &lt; 0.03). Twenty five (29%) patients had IR and this could be accounted for by the APR and body mass index (BMI). Cholesterol/HDL-cholesterol ratios were elevated and this was only partially attributable to the APR, BMI and IR. Twenty four (28%) patients had decreased DHEAS concentrations and in women, this could not be fully explained by the APR, IR, disease duration, previous glucocorticoid and current NSAID usage. <h3>Conclusion</h3> Further elucidation of etiopathogenetic mechanisms shared by IP and CVD may yield more effective therapies for both conditions. Meanwhile, CVD risk factor profiles should be addressed in IP management. <h3>References</h3> Dessein PH, et al. Rheumatology 2001, in press Liuzzo G, et al. Circulation 2000;102: 2883–8 Weyand CM, et al. Arch Immunol Ther Exp (Warsz) 2000;48:429–35 Kroot EJ, <i>et al</i>. Ann Rheum Dis. 2000;59:954–8
Persistent STAT5 activation reprograms the epigenetic landscape in CD4 <sup>+</sup> T cells to drive polyfunctionality and antitumor immunity
Authors: Zhi-Chun Ding, Huidong Shi, Nada S. Aboelella, Kateryna Fesenkova, Eun-Jeong Park, Zhuoqi Liu, Lirong Pei, Jiaqi Li, Richard A. McIndoe, Hongyan Xu, Gary A. Piazza, Bruce R. Blazar, David H. Munn, Gang Zhou
Journal: Science Immunology (2020)

The presence of polyfunctional CD4+ T cells is often associated with favorable antitumor immunity. We report here that persistent activation of signal transducer and activator of transcription 5 (STAT5) in tumor-specific CD4+ T cells drives the development of polyfunctional T cells. We showed that ectopic expression of a constitutively active form of murine STAT5A (CASTAT5) enabled tumor-specific CD4+ T cells to undergo robust expansion, infiltrate tumors vigorously, and elicit antitumor CD8+ T cell responses in a CD4+ T cell adoptive transfer model system. Integrated epigenomic and transcriptomic analysis revealed that CASTAT5 induced genome-wide chromatin remodeling in CD4+ T cells and established a distinct epigenetic and transcriptional landscape. Single-cell RNA sequencing analysis further identified a subset of CASTAT5-transduced CD4+ T cells with a molecular signature indicative of progenitor polyfunctional T cells. The therapeutic significance of CASTAT5 came from our finding that adoptive transfer of T cells engineered to coexpress CD19-targeting chimeric antigen receptor (CAR) and CASTAT5 gave rise to polyfunctional CD4+ CAR T cells in a mouse B cell lymphoma model. The optimal therapeutic outcome was obtained when both CD4+ and CD8+ CAR T cells were transduced with CASTAT5, indicating that CASTAT5 facilitates productive CD4 help to CD8+ T cells. Furthermore, we provide evidence that CASTAT5 is functional in primary human CD4+ T cells, underscoring its potential clinical relevance. Our results implicate STAT5 as a valid candidate for T cell engineering to generate polyfunctional, exhaustion-resistant, and tumor-tropic antitumor CD4+ T cells to potentiate adoptive T cell therapy for cancer.
Impact of Measurable Residual Disease (MRD) By Multiparameter Flow Cytometry (MFC): A Real-World Study in 1,076 Patients with Acute Myeloid Leukemia (AML)
Authors: Bruno Paiva, María Belén Vidriales, Maria Desamparados Sampere Talens, Fabian Tarin, Enrique Colado, Celina Benavente, María Teresa Cedena, Joaquin Sanchez, Teresa Caballero-Velázquez, Lourdes Cordon, David Martínez-Cuadron, Teresa Bernal del Castillo, Carmen Botella, Sofia Grille, Josefina Serrano, Carlos Rodriguez, Jesús Lorenzo Algarra, Juan Manuel Alonso Dominguez, Maria Luz Amigo, Manuel BARRIOS García, Raimundo García-Boyero, Mercedes Colorado, Jaime Perez De Oteyza, Manuel Perez Encinas, Lissette Del Pilar Costilla, Maria Jose Sayas, Olga Pérez-López, Marcos González, Jose A. Perez-Simon, Joaquin Martinez-Lopez, Claudia Lucia Sossa, Alberto Orfao, Jesús F. San-Miguel, Miguel Sanz, Pau Montesinos
Journal: Blood (2020)
Actions of L-Glutamine vs. COVID-19 Suggest Additional Benefit in Sickle Cell Disease
Authors: Mahmoud A.Z. Abdelaal, Dyala Abdelrahman, Mahir Cengiz, Hakan Yavuzer, Serap Yavuzer, Ivy Bien, Preeti Bhuva, Jessica V Pham, Royal Siu, Mengdi Tang, Ashley Ward, Jason Goodrow, Peter Ludlum, Charles W. Stark, Susan P. Perrine
Journal: Blood (2020)
Abstract 10882: Outcomes of Prospective ICD Reprogramming to Reduce Risk of Unnecessary ICD Therapy
Authors: Matthew Martini, Matthew Kalscheur, Miguel A Leal, Erin Dehn, Teri McSherry, Timothy Hess, Ryan T Kipp
Journal: Circulation (2019)

Introduction: Prospective studies have shown that programming Implantable Cardioverter Defibrillators (ICDs) at device implantation with high rate therapy or delayed therapy reduces the rate of unn...
THU0085 Il-15 enhances expression of mrna encoding anti-apoptotic protein bcl-xl and triggers proliferation of rheumatoid arthritis fibroblast like synoviocytes
Authors: MS Kurowska, E Kontny, I Janicka, W Rudnicka, J Kowalczewski, W Maslinski
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> The hallmarks of rheumatoid arthritis (RA) are leukocytic infiltration of the synovium and expansiveness of fibroblast like synoviocytes (FLS). The abnormal proliferation of FLS as well as their resistance for apoptosis is thought to be mediated, at least in part, by the overproduction of proinflammatory cytokines and growth factors. IL-15, a T-cell growth factor, has been suggested to play an important role in the pathogenesis of RA. In the present study we tested the hypothesis that IL-15 contributes to FLS expansiveness. <h3>Objectives</h3> The aim of this study was to: (i) examine whether RA-FLS express all three receptor chains, i.e. IL-15Ra, IL-2Rb and IL-2Rg required for functional IL-15 receptor complex; (ii) investigate the effect of IL-15 on RA-FLS proliferation; and (iii) analyse IL-15 triggered expression of mRNA encoding anti-apoptotic: Bcl-xL and Bcl-2, and proapoptotic Bcl-xS proteins in these cells. <h3>Methods</h3> Synoviocytes isolated from synovial membrane of RA patients (cultured for 2–7 passages) or PBMC from healthy donors were stimulated with TNF-a (10 ng/ml), IL-1b (1ng/ml) or IL-15 (25 ng/ml) in medium supplemented with 5% or 0.1% FCS. After 4 h stimulation, levels of mRNA encoding IL-15Ra, IL-2Rb, IL-2Rg, Bcl-2, Bcl-xS and Bcl-xL were analysed by RT-PCR. The expression of surface IL-15Ra was tested using flow cytometry after 24–48 h stimulation. Proliferation of the FLS was determined based on the incorporation of 3H-thymidine after 72 h pretreatment with 0.1% FCS then 24 h stimulation with IL-15 in medium with 0.1% FCS. <h3>Results</h3> Human FLS express mRNA encoding IL-15Ra isoforms and IL-2Rb and g chains. Interestingly, TNF-a or IL-1 b trigger significant elevation of mRNA encoding IL-15Ra isoforms (3 times), but not IL-2Rb or g chains. Flow cytometric analysis confirmed the enhancement of IL-15Ra protein expression. The IL-15 receptor complex is functional: IL-15 increased (by ~ 68%) proliferation of FLS in medium with low (0.1%) FSC. Moreover, in these conditions, IL-15 triggers significant elevation of mRNA encoding anti-apoptotic protein Bcl-xL, while the pro-apoptotic Bcl-xS remained unchanged. However, unlike in PBMC, IL-15 fails to rise the level of anti-apoptotic bcl-2 mRNA in FLS. <h3>Conclusion</h3> Our studies indicate that IL-15, via enhancement of anti-apoptotic Bcl-xL and increased proliferation is, at least in part, responsible for expansive behaviour of FLS.
Single Cell Transcriptomics Revealed AML and Non-AML Cell Clusters Relevant to Relapse and Remission in Pediatric AML
Authors: Beena E Thomas, Pruthvi Perumalla, Swati S Bhasin, Debasree Sarkar, Bhakti Dwivedi, Sunita I Park, Deborah DeRyckere, Curtis J. Henry, Sunil S. Raikar, Christopher C. Porter, Melinda Pauly, Ryan J Summers, Sharon M. Castellino, Daniel S. Wechsler, Douglas K Graham, Manoj Bhasin
Journal: Blood (2020)
Abstract #4650: Development of human blocking antibodies to \#916;-like ligand-4 (Dll4) in VelocImmune mice for anti-angiogenesis therapy
Authors: Irene Noguera-Troise, Nicholas Papadopoulos, Eric Smith, Sandra Coetzee, Carlos Hickey, Tammy Huang, Joel Martin, Andrew Murphy, David Valenzuela, James Fandl, Gang Chen, Sam Davis, Neil Stahl, George Yancopoulos, Gavin Thurston
Journal: Cancer Research (2009)

The growth of solid tumors depends on the growth of a functional tumor vasculature. Recent studies have shown that blockade of the Dll4-Notch pathway in established tumors results in increased tumor vessel density, but paradoxically, increased tumor hypoxia and decreased tumor growth, even in tumors that are resistant to VEGF blockade. These anti-tumor actions of Dll4 blockade are a result of aberrant non-productive tumor angiogenesis. To exploit Dll4 as a target for the treatment of cancer, we sought to develop and characterize fully human antibodies that block the Dll4-Notch pathway. By immunizing VelocImmune mice, which express the full repertoire of human antibody variable domains in the endogenous locus of the mouse immunoglobin gene, we discovered an array of antibodies that bind to various domains of Dll4 and efficiently block the interaction of Dll4 with Notch receptors. Further characterization was performed on 40 of these antibodies, which represent significant diversity of repertoire and bind Dll4 with an affinity of less than 1 nM, in cell-based and biochemical assays. A subset of these antibodies was further tested using in vivo assays. To better evaluate the effects of these antibodies in pre-clinical tumor models, we used Velocigene technology to generate a genetically engineered mouse in which the region of the murine Dll4 gene that encodes the extracellular portion of Dll4 was replaced with the equivalent human genetic region (~7 kB). This \#8216;humanized\#8217; Dll4 allele expresses Dll4 mRNA and protein at approximately the same levels as the endogenous allele and has yielded viable homozygous mice. Initial studies in these humanized Dll4 mice demonstrate that VelocImmune Dll4 antibodies potently inhibit tumor growth and produce aberrant tumor vasculature. These novel reagents will allow for detailed evaluation of the role of Dll4 in tumor angiogenesis, as well as meaningful characterization of fully human Dll4 antibodies for pre-clinical development.  Citation Information: In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 4650.
Clinicopathologic Correlates and Natural History of Atypical Chronic Myeloid Leukemia
Authors: Guillermo Montalban Bravo, Rashmi Kanagal-Shamanna, Koji Sasaki, Lucia Masarova, Kiran Naqvi, Elias Jabbour, Courtney D. DiNardo, Koichi Takahashi, Marina Konopleva, Naveen Pemmaraju, Nicholas J. Short, Ghayas C. Issa, Tapan M. Kadia, Farhad Ravandi, Naval Daver, Gautam Borthakur, Zeev E. Estrov, Joseph D. Khoury, Sanam Loghavi, Sherry A. Pierce, Carlos E. Bueso-Ramos, Keyur Patel, Srdan Verstovsek, Hagop M. Kantarjian, Prithviraj Bose, Guillermo Garcia-Manero
Journal: Blood (2020)
Abstract 513: Emre Regulates the Mitochondrial Calcium Uniporter <i>in vivo</i>
Authors: Julia C Liu, Nicole Syder, Nima Ghorashi, Thomas B Willingham, Randi J Parks, Junhui Sun, Maria Fergusson, Jie Liu, Kira M Holmstrom, Sara Menazza, Danielle Springer, Chengyu Liu, Brian Glancy, Toren Finkel, Elizabeth Murphy
Journal: Circulation Research (2020)

Mitochondrial uptake of Ca 2+ plays critical roles in cardiac energy production as well as cell death. The mitochondrial calcium uniporter in mice and humans is a multi-protein complex that includes the channel-forming protein MCU and several other subunit proteins, including EMRE. EMRE is a single transmembrane protein that is conserved among metazoan species and is known to be essential for mitochondrial Ca 2+ uptake in cell culture. To investigate EMRE’s role in organismal physiology, we generated a mouse model of global germline EMRE deletion. We show that EMRE is indeed required for mitochondrial calcium uniporter function in isolated mitochondria from multiple tissues. Although the birth rate of Emre -/- mice is lower than expected by Mendelian genetics (~5-10% instead of ~25%), the mice that are born are viable and appear healthy. Oxygen consumption in isolated mitochondria and cells is not significantly affected by loss of EMRE, and similarly the mice do not exhibit overt metabolic impairment, even under strenuous exercise. No significant differences between Emre -/- and wild-type ( WT ) cardiac function at baseline and after isoproterenol stimulation are evident by echocardiography. Moreover, Emre -/ - hearts are not protected from ischemia/reperfusion injury in a Langendorff perfusion model (mean infarct area 61% in Emre -/- hearts; 57% in WT ). Collectively, these data and their similarities to results found via germline Mcu deletion demonstrate that EMRE is indeed essential for mitochondrial Ca 2+ uptake in vivo. Furthermore, we find evidence that EMRE protein expression is elevated in some mouse muscular dystrophy models, suggesting that modulation of EMRE levels may play a role in regulating uniporter activity in conditions of stress or disease. We therefore further explore whether and how EMRE expression changes with isoproterenol-induced cardiac hypertrophy in mice and in samples from human patients with heart failure. Understanding of how uniporter components such as EMRE can regulate MCU in a diseased state can inform better therapeutic strategies aimed at restoring mitochondrial metabolic homeostasis.
Risk Factors Associated with 30-Day Unplanned Readmissions for Adult Acute Lymphoblastic Leukemia (ALL)
Authors: Veronica A Guerra, Yasmin Alwash, Yan Yuanqing, Jorge M. Ramos Perez, Guillaume Richard-Carpentier, Ahmad S. Alotaibi, Hycienth O Ahaneku, Bachar Samra, Arrvind Raghunath, Nitin Jain, Nicholas J. Short, Farhad Ravandi, Gautam Borthakur, Alessandra Ferrajoli, Koji Sasaki, Steven M. Kornblau, Zeev E. Estrov, Jorge E. Cortes, Hagop M. Kantarjian, Guillermo Garcia-Manero, Elias Jabbour, Tapan M. Kadia
Journal: Blood (2020)
An Autoimmunogenic and Proinflammatory Profile Defined by the Gut Microbiota of Patients With Untreated Systemic Lupus Erythematosus
Authors: Bei‐di Chen, Xin‐miao Jia, Jia‐yue Xu, Li‐dan Zhao, Jun‐yi Ji, Bing‐xuan Wu, Yue Ma, Hao Li, Xiao‐xia Zuo, Wen‐you Pan, Xiao‐han Wang, Shuang Ye, George C. Tsokos, Jun Wang, Xuan Zhang
Journal: Arthritis & Rheumatology (2020)

Objective Changes in gut microbiota have been linked to systemic lupus erythematosus (SLE), but knowledge is limited. Our study aimed to provide an in‐depth understanding of the contribution of gut microbiota to the immunopathogenesis of SLE. Methods Fecal metagenomes from 117 patients with untreated SLE and 52 SLE patients posttreatment were aligned with 115 matched healthy controls and analyzed by whole‐genome profiling. For comparison, we assessed the fecal metagenome of MRL/ lpr mice. The oral microbiota origin of the gut species that existed in SLE patients was documented by single‐nucleotide polymorphism–based strain‐level analyses. Functional validation assays were performed to demonstrate the molecular mimicry of newly found microbial peptides. Results Gut microbiota from individuals with SLE displayed significant differences in microbial composition and function compared to healthy controls. Certain species, including the Clostridium species ATCC BAA‐442 as well as Atopobium rimae , Shuttleworthia satelles , Actinomyces massiliensis , Bacteroides fragilis , and Clostridium leptum , were enriched in SLE gut microbiota and reduced after treatment. Enhanced lipopolysaccharide biosynthesis aligned with reduced branched chain amino acid biosynthesis was observed in the gut of SLE patients. The findings in mice were consistent with our findings in human subjects. Interestingly, some species with an oral microbiota origin were enriched in the gut of SLE patients. Functional validation assays demonstrated the proinflammatory capacities of some microbial peptides derived from SLE‐enriched species. Conclusion This study provides detailed information on the microbiota of untreated patients with SLE, including their functional signatures, similarities with murine counterparts, oral origin, and the definition of autoantigen‐mimicking peptides. Our data demonstrate that microbiome‐altering approaches may offer valuable adjuvant therapies in SLE.
Phase 1 Study of CD19 Targeted 4-1BBL Costimulatory Agonist to Enhance T Cell (Glofitamab Combination) or NK Cell Effector Function (Obinutuzumab Combination) in Relapsed/Refractory B Cell Lymphoma
Authors: Martin Hutchings, Fritz C. Offner, Francesc Bosch, Giuseppe Gritti, Carmelo Carlo-Stella, Harriet Walter, William Townsend, Franck Morschhauser, Guillaume Cartron, Hervé Ghesquieres, Sophie de Guibert, Sylvia Herter, Koorosh Korfi, Veronica Craine, Sarah Louise Mycroft, Matt Whayman, Claudia Mueller, Natalie Dimier, Tom Moore, Sara Belli, Martin Kornacker, Katharina Lechner, Michael Dickinson
Journal: Blood (2020)
Thrombotic Events and Mortality Risk in Patients Newly Diagnosed with Intermediate- to High-Risk Essential Thrombocythemia in the United States
Authors: Naveen Pemmaraju, Aaron T. Gerds, Jingbo Yu, Shreekant Parasuraman, Anne Shah, Ann Xi, Shambhavi Kumar, Robyn M. Scherber, Srdan Verstovsek
Journal: Blood (2020)
Generation of Multiplexed Engineered, Off-the-Shelf CAR T Cells Uniformly Carrying Multiple Anti-Tumor Modalities to Prevent Tumor Relapse
Authors: Chiawei Chang, Eigen Peralta, Gloria Hsia, Bi-Huei Yang, Wen-I Yeh, Raedun Clarke, Mandal Mili, Tom Lee, Mochtar Pribadi, Ramzey Abujarour, Yi-Shin Lai, David Robbins, Matthew Denholtz, Sandeep Kothapally Hanok, Emily Driver, Emily Carron, Natalie Navarrete, May Sumi, Amit Mehta, Philip Chu, Jason ORourke, Alma Gutierrez, Eric Sung, Suzanna Gasparian, Angela Gentile, Alec Witty, Amanda Yzaguirre, Samuel LaBarge, Cokey Nguyen, Bahram Valamehr
Journal: Blood (2020)