tbuckley/cabot-search huggingface dataset:
Abstract 482: Beta-catenin Activation in Cardiac Fibroblasts Modulates the Immune Micro-environment to Promote Fibrosis and Heart Failure Following Chronic Injury
Authors: Meiling Melzer, Dina Hassan, David Beier, Pampee P Young, Sarika Saraswati
Journal: Circulation Research (2020)

Almost 6.5 million people in United States suffer from heart failure (HF). Diastolic HF following non-ischemic cardiac insult is a progressive condition with limited effective therapies underscoring the urgency to invest in identifying novel therapeutic targets for treatment. Reactive fibrosis in response to pathological stress is one of the major causes of diastolic HF. Emerging data suggest an association of systemic inflammation with reactive fibrosis and HF. Canonical Wnt/beta-catenin signaling has been linked to HF and fibrosis with limited understanding of the precise cellular and molecular mechanism. We utilized thoracic aortic constriction (TAC), a well-defined model of HF, to study Wnt signaling mediated reactive fibrosis. TAC was induced in a transgenic mouse model with stabilized beta-catenin (Wnt signaling) in fibroblasts (Bcat/Postn). Wnt activation following TAC resulted in increased maladaptive reactive fibrosis, HF marker ANP, and cardiac hypertrophy with preserved Ejection Fraction (pEF) suggesting Wnt-mediated progression of diastolic heart failure with pEF. TAC also resulted in increased macrophage activation and recruitment of CD8+ cytotoxic T-cells. In vitro co-culture of Wnt3a-overexpressing fibroblasts with activated myeloid cells promoted fibroblast proliferation and collagen synthesis. Therefore, we hypothesize that Wnt signaling activation promotes interstitial fibrosis via recruitment of specific inflammatory cells. Genomic analysis further supports this by demonstrating distinct chemokine gene expression patterns in fibroblasts resulting from Wnt activation in these injury models. Our future goal is to elucidate the role of Wnt signaling in modulating the fibroblast-immune cell crosstalk in modulating interstitial fibrosis induced diastolic HFpEF. Currently, there is no approved therapy to specifically target reactive fibrosis to avert diastolic dysfunction. Our study is aiming to identify targetable cellular and molecular players that improve, prevent or avert reactive fibrosis mediated HFpEF in order to reduce the incidence and severity of pathology resulting from HF.
Clinical Characteristics, Immunophenotype and Outcomes of Blastic Plasmacytoid Dendritic Cell Neoplasms in a Peruvian Cohort
Authors: Daniela Dueñas, Elizabeth Cervantes, Daniel J Enriquez, Claudio Flores, Carlos Barrionuevo, Cindy Alcarraz, Lourdes Lopez, Shirley Quintana, Jule F Vasquez, Rosario Retamozo, Judith Vidal, Tatiana Saldarriaga, Antonio A Carrasco-Yalán, Juan L Garcia-Leon, Cesar Samanez-Figari
Journal: Blood (2020)
Clinical Relevance of Morphologic and Molecular Complete Remission in AML Patients Undergoing Reduced Intensity or Non-Myeloablative Conditioning
Authors: Madlen Jentzsch, Dominic Brauer, Juliane Grimm, Marius Bill, Donata Backhaus, Julia Schulz, Dietger Niederweiser, Uwe Platzbecker, Sebastian Schwind
Journal: Blood (2020)
Sarcopenia – Molecular mechanisms and open questions
Authors: Petra Wiedmer, Tobias Jung, José Pedro Castro, Laura C.D. Pomatto, Patrick Y. Sun, Kelvin J.A. Davies, Tilman Grune
Journal: Ageing Research Reviews (2020)

Sarcopenia represents a muscle-wasting syndrome characterized by progressive and generalized degenerative loss of skeletal muscle mass, quality, and strength occurring during normal aging. Sarcopenia patients are mainly suffering from the loss in muscle strength and are faced with mobility disorders reducing their quality of life and are, therefore, at higher risk for morbidity (falls, bone fracture, metabolic diseases) and mortality. Several molecular mechanisms have been described as causes for sarcopenia that refer to very different levels of muscle physiology. These mechanisms cover e. g. function of hormones (e. g. IGF-1 and Insulin), muscle fiber composition and neuromuscular drive, myo-satellite cell potential to differentiate and proliferate, inflammatory pathways as well as intracellular mechanisms in the processes of proteostasis and mitochondrial function. In this review, we describe sarcopenia as a muscle-wasting syndrome distinct from other atrophic diseases and summarize the current view on molecular causes of sarcopenia development as well as open questions provoking further research efforts for establishing efficient lifestyle and therapeutic interventions.
Abstract 293: Functional Recovery After Gene Therapy and Hippo Pathway Knock Down After Myocardial Infarction in a Pig Model
Authors: Shijie Liu, Ke Li, Todd Heallen, Li Tang, Yidan Wang, Leonardo Wagner, James T Willerson, Emerson C Perin, Sui Zhang, James F Martin
Journal: Circulation Research (2020)

Heart failure (HF), a devastating disease and a leading cause of death worldwide, is an unmet clinical need. The Hippo pathway, an inhibitory kinase cascade, represses adult cardiomyocyte (CM) proliferation post-myocardial infarction (MI) in rodent models. Here, we investigated an Adeno Associated Virus 9 (AAV9) gene therapy that knocks down the Hippo pathway gene, Sav, in a pig model of MI after ischemic reperfusion (I/R), to closely model the human condition. Two weeks post-MI, when pigs had established left ventricular (LV) systolic dysfunction, we delivered an AAV9- Sav -shRNA or control virus by subendocardial injections to border zone (BZ) CMs. Three months post viralinjections, AAV9- Sav -shRNA injected pigs had improved LV systolic function, evidence of CM division, and reduced scar size. In addition, AAV9- Sav- shRNA treated hearts had more capillaries and reduced CM ploidy. AAV9- Sav -shRNA therapy was well tolerated without any mortality and pathologic examination of liver and lungs failed to uncover evidence for tumor formation revealing that AAV9- Sav -shRNA gene therapy is safe within the timeframe of this study. Our findings indicate that gene therapy, knocking down the Hippo pathway post-MI, in a pig model improves heart function and may have utility for humans.
Clinical Utility of Change in Nonalcoholic Fatty Liver Disease Activity Score and Change in Fibrosis in NAFLD
Authors: Nobuharu Tamaki, Nagambika Munaganuru, Jinho Jung, Aed Qas Yonan, Richele Bettencourt, Veeral Ajmera, Mark A. Valasek, Cynthia Behling, Rohit Loomba
Journal: Clinical Gastroenterology and Hepatology (2020)
Age-Associated Changes in Bone Marrow-Derived Extracellular Vesicles May Alter Their Effects on Murine Hematopoietic Stem Cell Function
Authors: Sicheng Wen, Jill Kreiling, Mark S Dooner, Elaine Papa, Mandy Pereira, Michael Del Tatto, Yan Cheng, Peter J Quesenberry, Laura R Goldberg
Journal: Blood (2020)
Karonudib Has Potent Anti-Tumor Effects in Preclinical Models of B-Cell Lymphoma
Authors: Morten P Oksvold, Ulrika Warpman Berglund, Helge Gad, Baoyan Bai, Trond Stokke, Idun D Rein, Therese Pham, Kumar Sanjiv, Geir Frode Øy, Jens Henrik Norum, Erlend B. Smeland, June Helen Myklebust, Thomas Helleday, Thea Kristin Våtsveen
Journal: Blood (2020)
CXCR4 PET imaging of mantle cell lymphoma using [<sup>68</sup>Ga]Pentixafor: comparison with [<sup>18</sup>F]FDG-PET
Authors: Marius E. Mayerhoefer, Markus Raderer, Wolfgang Lamm, Verena Pichler, Sarah Pfaff, Michael Weber, Barbara Kiesewetter, Markus Hacker, Lukas Kazianka, Philipp B. Staber, Hans-Juergen Wester, Johannes Rohrbeck, Ingrid Simonitsch-Klupp, Alexander Haug
Journal: Theranostics (2020)

For PET imaging of mantle cell lymphoma (MCL), [18F]FDG (2-deoxy-2-[18F]fluoro-D-glucose) is the currently recommended radiotracer, although uptake is variable and bone marrow evaluation is limited. In this prospective study, we evaluated the novel CXCR4 (G-protein-coupled C-X-C chemokine receptor type 4) tracer [68Ga]Pentixafor in MCL patients, and compared it to [18F]FDG. Methods: MCL patients underwent [68Ga]Pentixafor-PET/MRI, and, if required for routine purposes, also [18F]FDG-PET/MRI, before treatment. PET was evaluated separately for 23 anatomic regions (12 lymph node stations and 11 organs/tissues), using MRI as the main reference standard. Standardized uptake values (SUVmax and SUVmean) and tumor-to-background ratios (TBRblood and TBRliver) were calculated. General Estimation Equations (GEE) were used to compare [68Ga]Pentixafor-PET and [18F]FDG-PET sensitivities and positive predictive values (PPV). For bone marrow involvement, where biopsy served as the main reference standard, and splenic involvement, receiver operating characteristic curves were used to determine the optimal SUV and TBR cut-off values, and areas under the curve (AUC) were calculated. Results: Twenty-two MCL patients were included. [68Ga]Pentixafor-PET sensitivity (100%) was significantly higher than for [18F]FDG-PET (75.2%) (P<0.001), and PPV was slightly, but not significantly lower (94.0%.vs. 96.5%; P=0.21). SUVs and TBRs were significantly higher for [68Ga]Pentixafor-PET than for [18F]FDG-PET (P<0.001 in all cases); the greatest difference was observed for mean TBRblood, with 4.9 for [68Ga]Pentixafor-PET and 2.0 for [18F]FDG-PET. For bone marrow involvement, [68Ga]Pentixafor-PET SUVmean showed an AUC of 0.92; and for splenic involvement, TBRblood showed an AUC of 0.81. Conclusion: [68Ga]Pentixafor-PET may become an alternative to [18F]FDG-PET in MCL patients, showing clearly higher detection rates and better tumor-to-background contrast.
A Comprehensive High Resolution Scrna-Seq Analytical Platform for Characterizing Human Hematopoietic Stem/Progenitor Cells States in Ex Vivo Drug Products
Authors: Cristina Baricordi, Mariana Loperfido, Aimin Yan, Luigi Barbarossa, Mercedes Segura, Azadeh Golipour, Chris Mason, Luca Biasco
Journal: Blood (2020)
Pharmacology and Pharmacokinetics of NXT007; Emicizumab-Based Engineered Fixa/Fx Bispecific Antibody with Improved Properties
Authors: Kazuki Yamaguchi, Tetsuhiro Soeda, Motohiko Sato, Norihito Shibahara, Hikaru Koga, Mina Ichiki, Eri Joyashiki, Yuri Teranishi, Kei Nishimura, Hirotake Shiraiwa, Hidetomo Kitamura, Tomoyuki Igawa, Hiroko Konishi, Takehisa Kitazawa
Journal: Blood (2020)
Abstract 460: Cyclin Dependent Kinase Inhibitor A1 Identified as a Potential Risk Locus for Hypertrophic Cardiomyopathy
Authors: Alex Gyftopoulos, Yi-Ju Chen, Libin Wang, Charles H Williams, Young Wook Chun, James A Perry, Charles C Hong
Journal: Circulation Research (2020)

Hypertrophic cardiomyopathy (HCM) is characterized by heterogeneous phenotypic expression, natural history, and genetic profile with numerous causative mutations. The relationship between genotype and phenotype in HCM is incompletely understood. Identifying genetic modifiers may expand understanding of the signaling pathways that are responsible for phenotypic expression. UK Biobank comprises clinical and genetic data for greater than 500,000 individuals. We compared control individuals to those with a diagnosis of HCM (identified via ICD-10 code I42.1) in a 20-to-1 fashion to identify genetic differences. Data were compared using Mixed Model Analysis for Pedigrees/Populations (MMAP) mixed-model regression. Variants were assessed using bioinformatics tools including linkage disequilibrium and Eigen scoring. Results were then compared to previously published genome-wide association datasets. Mixed-model regression identified 5 variants of cyclin-dependent kinase inhibitor 1A ( CDKN1A ) as statistically significant with one intronic variant (rs3176326) likely affecting a gene promoter region with an Eigen-PC score of 7.779. This variant was found to have a p-value of 5.08x10 -8 when contrasted to controls with a minor allele frequency of 0.199 in the affected individuals. The 4 other variants were in linkage disequilibrium (r 2 0.90-0.99) with rs3176326. The odds ratio of HCM with rs3176326 is 1.81.To our knowledge, CDKN1A has not previously been associated with HCM. By utilizing bioinformatic tools we were able to identify 5 variants that may be associated with the risk for HCM. One locus affects a promotor region and resulted in a notably high Eigan-PC score suggestive that it has an impact on HCM. When comparing these findings with previous genome-wide association studies utilizing the UK Biobank, we find that CDKN1A has a possible association with HCM, though those results were not statistically significant. CDKN1A has been previously associated with the p53 DNA repair and cell senescence pathway. Animal and human studies have implicated it in the development of fibrosis. A recent genome-wide association metanalysis identified it as a risk locus for heart failure. These findings support our conclusion that CDKN1A is a risk locus for HCM.
Rapid Engraftment, Immune Cell Reconstitution and Sustained Donor Chimerism in Patients Receiving G-CSF Mobilized Peripheral Blood Stem Cells (PB-SC) from Related or Unrelated Donors Undergoing CD34 Enrichment with Mononuclear Cell (T cell) Addback in Children, Adolescents, and Adults with Malignant and Nonmalignant Diseases
Authors: Jordan Milner, Cydney Nichols, Janet Ayello, Karen P. Seiter, Delong Liu, Erin Morris, Sandra Fabricatore, Yaya Chu, Rosemarie Shaw, Carmella van de Ven, Allyson M. Flower, Mitchell S Cairo
Journal: Blood (2020)
Enhancing the Immune Surveillance in Multiple Myeloma Via CDK4/6 Inhibition
Authors: Yan Xu, Yao Yao, Woojun Daniel Park, Sanika Derebail, Chandraditya Chakraborty, Shidai Mu, Rafael Alonso Fernández, Srikanth Talluri, Zuzana Chyra, Kenneth Wen, Qingsheng Yan, Osasenaga Idahor, Selene Cipri, Rao Prabhala, Kenneth Anderson, Mehmet K. Samur, Mariateresa Fulciniti, Nikhil C. Munshi
Journal: Blood (2020)
The Addition of Venetoclax to Ibrutinib Achieves a High Rate of Undetectable Minimal Residual Disease in Patients with High-Risk CLL
Authors: Philip A. Thompson, Alessandra Ferrajoli, Nitin Jain, Yan Wang, Christine B Peterson, Naveen Garg, Chongjuan Wei, Ana Ayala, Tapan M. Kadia, Prithviraj Bose, Naveen Pemmaraju, Nicholas J. Short, Michael J. Keating, William G. Wierda
Journal: Blood (2020)
Breast Cancer Index Predicts Extended Endocrine Benefit to Individualize Selection of Patients with HR+ Early-stage Breast Cancer for 10 Years of Endocrine Therapy
Authors: Iris Noordhoek, Kai Treuner, Hein Putter, Yi Zhang, Jenna Wong, Elma Meershoek-Klein Kranenbarg, Marjolijn Duijm-de Carpentier, Cornelis J.H. van de Velde, Catherine A. Schnabel, Gerrit-Jan Liefers
Journal: Clinical Cancer Research (2020)

Individualized selection of patients with early-stage hormone receptor-positive (HR+) breast cancer for extended endocrine therapy (EET) is required to balance modest gains in outcome with toxicities of prolonged use. This study examined the Breast Cancer Index [BCI; HOXB13/IL17BR ratio (H/I)] as a predictive biomarker of EET benefit in patients from the Investigation on the Duration of Extended Adjuvant Letrozole trial.BCI was tested in primary tumor specimens from 908 patients randomized to receive 2.5 versus 5 years of extended letrozole. The primary endpoint was recurrence-free interval. Cox models and likelihood ratios tested the interaction between EET and BCI (H/I).BCI (H/I)-high significantly predicted benefit from extended letrozole in the overall cohort [HR 0.42; 95% confidence interval (CI), 0.21-0.84; P = 0.011] and any aromatase inhibitor subset [HR 0.34; 95% CI, 0.16-0.73; P = 0.004), whereas BCI (H/I)-low patients did not derive significant benefit (HR 0.95; 95% CI, 0.58-1.56; P = 0.84 and HR 0.90; 95% CI, 0.53-1.55; P = 0.71, respectively) treatment to biomarker interaction was significant (P = 0.045, P = 0.025, respectively). BCI identified approximately 50% of patients with clinically high-risk disease that did not benefit, and with clinically low-risk disease that derived significant benefit, from an additional 2.5 years of EET.BCI (H/I) predicted preferential benefit from 5 versus 2.5 years of EET and identified patients with improved outcomes from completing 10 years of adjuvant endocrine therapy. Findings expand the clinical utility of BCI (H/I) to a broader range of patients and beyond prognostic risk factors as a predictive endocrine response biomarker for early-stage HR+ breast cancer.
Clinical Effectiveness of Combination Immunotherapy DPX-Survivac, Low Dose Cyclophosphamide, and Pembrolizumab in Recurrent/Refractory DLBCL: The Spirel Study
Authors: Neil L Berinstein, Isabelle Bence-Bruckler, Nicholas Allen Forward, Pierre Laneuville, Joy Mangel, Douglas A. Stewart, Irina Amitai, Gail Klein, Nancy Pennell, Iran Rashedi, Kim Roos, Yogesh Bramhecha, Rebekah Conlon
Journal: Blood (2020)
Management and Outcomes of Diffuse Large B Cell Lymphoma Post-Transplant Lymphoproliferative Disorder in the PET/CT Era: A Multicentre Study from the Australasian Lymphoma Alliance
Authors: Stephen Boyle, Joshua W.D. Tobin, Jacinta Perram, Nada Hamad, Allison Barraclough, Lydia Singaraveloo, Min-Hi Han, Richard Blennerhassett, Niles Elizabeth Nelson, Anna Johnston, Dipti Talaulikar, Krishna Karpe, Abir Bhattacharyya, Chan Yoon Cheah, Elango Subramoniapillai, Waqas Bokhari, Cindy Lee, Eliza A Hawkes, Veena Gullapalli, Andrew Jabbour, Simone Strasser, Steve Chadban, Christina Brown, Peter Mollee, Greg Hapgood
Journal: Blood (2020)
Abstract 534: Chemically Defined Cell Culture Media for High Yield Differentiation of Functional Human Cardiac Myocytes
Authors: Davi M Lyra Leite, Paul W Burridge
Journal: Circulation Research (2020)

Introduction: Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) are a promising technology for regenerative medicine and pharmacology. However, existing protocols are limited due to the high costs when generating cells at scale, to low yield, and to a lack of protocol replicability. Additionally, the use of animal-derived or recombinant proteins in cell differentiation creates concerns in human compatibility and presents technical challenges due to batch-to-batch variability. Aim: Develop a protocol for functional hiPSC-CM differentiation with high yield without the use of proteins. Methods: We expanded the CDM3 protocol by testing approximately 200 combinations of cell culture media during hiPSC differentiation. The differentiation was induced with a 24h incubation in 6 μM CHIR (d0), followed by 24 h in basal media (d1) and 48h in media supplemented with AA2P and Wnt-C59 (d2-d4). From day 4 onwards, cells were kept in media supplemented with insulin and AA2P, and in some conditions with polyvinyl alcohol. On day 8, hiPSC-CMs were antibiotically selected using geneticin. Tissues were imaged on day 13 to assess myocyte morphology and contraction. Videos were scored from 0 (dead/delaminated cells) to 9 (confluent tissues beating at least 4 times in a 5 sec interval). Results: We identified 6 basal media combinations that yield confluent monolayers on day 13. Out of these, 3 conditions consistently resulted in confluent contractile tissues. Conclusions: Our data demonstrate that a protein-free high yield hiPSC-CM differentiation is possible with the appropriate selection of basal media based on cellular nutritional requirements.
CPX351 Has Short Remission Duration but Is an Effective Bridge to Allogeneic Transplant in High Risk AML: Results from Canadian Real-World Multi-Centre Study
Authors: Claire Andrews, Taylor Young, Eshetu G Atenafu, Sarit E Assouline, Joseph M Brandwein, Steven M Chan, Signy Chow, Dina Khalaf, Vikas Gupta, Dennis Dong Hwan Kim, Dawn Maze, Mark D. Minden, Caroline J McNamara, Tracy Murphy, David Sanford, Aaron D Schimmer, Andre C. Schuh, Karen W.L. Yee, Hassan Sibai
Journal: Blood (2020)
Gastrointestinal Events and Management Strategies for Patients with Acute Myeloid Leukemia (AML) in First Remission Receiving CC-486 in the Randomized, Placebo-Controlled, Phase III QUAZAR AML-001 Maintenance Trial
Authors: Farhad Ravandi, Christopher Pocock, Dominik Selleslag, Pau Montesinos, Hamid Sayar, Maurizio Musso, Angela Figuera Alvarez, Hana Safah, William Tse, Sang Kyun Sohn, Devendra K Hiwase, Timothy Chevassut, Francesca Pierdomenico, Ignazia La Torre, Barry Skikne, Keshava Kumar, Qian Dong, C.L. Beach, Hervé Dombret
Journal: Blood (2020)
Genomic Analysis of Vascular Invasion in HCC Reveals Molecular Drivers and Predictive Biomarkers
Authors: Maya S. Krishnan, Anand Rajan KD, Jangho Park, Vinodhini Arjunan, Fernando Jose Garcia Marques, Abel Bermudez, Olivia A. Girvan, Nam S. Hoang, Jun Yin, Mindie H. Nguyen, Nishita Kothary, Sharon Pitteri, Dean W. Felsher, Renumathy Dhanasekaran
Journal: Hepatology (2020)

Background and Aims Vascular invasion (VI) is a critical risk factor for HCC recurrence and poor survival. The molecular drivers of vascular invasion in HCC are open for investigation. Deciphering the molecular landscape of invasive HCC will help identify therapeutic targets and noninvasive biomarkers. Approach and Results To this end, we undertook this study to evaluate the genomic, transcriptomic, and proteomic profile of tumors with VI using the multiplatform cancer genome atlas (The Cancer Genome Atlas; TCGA) data (n = 373). In the TCGA Liver Hepatocellular Carcinoma cohort, macrovascular invasion was present in 5% (n = 17) of tumors and microvascular invasion in 25% (n = 94) of tumors. Functional pathway analysis revealed that the MYC oncogene was a common upstream regulator of the mRNA, miRNA, and proteomic changes in VI. We performed comparative proteomic analyses of invasive human HCC and MYC‐driven murine HCC and identified fibronectin to be a proteomic biomarker of invasive HCC (mouse fibronectin 1 [Fn1], P = 1.7 × 10 −11 ; human FN1, P = 1.5 × 10 −4 ) conserved across the two species. Mechanistically, we show that FN1 promotes the migratory and invasive phenotype of HCC cancer cells. We demonstrate tissue overexpression of fibronectin in human HCC using a large independent cohort of human HCC tissue microarray (n = 153; P &lt; 0.001). Lastly, we showed that plasma fibronectin levels were significantly elevated in patients with HCC (n = 35; mean = 307.7 μg/mL; SEM = 35.9) when compared to cirrhosis (n = 10; mean = 41.8 μg/mL; SEM = 13.3; P &lt; 0.0001). Conclusions Our study evaluates the molecular landscape of tumors with VI, identifying distinct transcriptional, epigenetic, and proteomic changes driven by the MYC oncogene. We show that MYC up‐regulates fibronectin expression, which promotes HCC invasiveness. In addition, we identify fibronectin to be a promising noninvasive proteomic biomarker of VI in HCC.
Pembrolizumab Monotherapy in Relapsed or Refractory Primary Mediastinal Large B-Cell Lymphoma (PMBCL): 3-Year Follow-up of the Keynote-170 Study
Authors: Pier Luigi Zinzani, Vladimir Melnichenko, Krimo Bouabdallah, Jan Walewski, Alejandro Majlis, Laura Fogliatto, Dolores Caballero, Beth A. Christian, Zafer Gulbas, Muhit Özcan, Gilles Salles, Margaret A. Shipp, Seth Thompson, Robert J Orlowski, Patricia Marinello, Philippe Armand
Journal: Blood (2020)
Determinants of Choice of Front-Line Tyrosine Kinase Inhibitor for Chronic Phase CML: A Study from the "Registro Italiano LMC &amp; Campus CML"
Authors: Mario Tiribelli, Roberto Latagliata, Massimo Breccia, Isabella Capodanno, Maria Cristina Miggiano, Francesco Cavazzini, Sabrina Leonetti Crescenzi, Sabina Russo, Mario Annunziata, Federica Sorà, Massimiliano Bonifacio, Giovanni Caocci, Giuseppina Loglisci, Alessandro Maggi, Gianni Binotto, Elena Crisà, Alessandra Iurlo, Anna Rita Scortechini, Annapaola Leporace, Rosaria Sancetta, Pamela Murgano, Concettina Ruggiero, Giuseppe Saglio, Giorgina Specchia
Journal: Blood (2020)
The Impact of Hemoglobin Level on Risk of End-Organ Damage among Patients with Sickle Cell Disease - A Large-Scale, Longitudinal Analysis
Authors: William B Ershler, Laura M De Castro, Zahra Pakbaz, Aaron Moynahan, Derek Weycker, Nhat Pham, Thomas E Delea, Irene Agodoa, Ze Cong
Journal: Blood (2020)