tbuckley/cabot-search huggingface dataset:
Preclinical and Clinical Signs of Efficacy of RVU120 (SEL120), a Specific CDK8/19 Inhibitor in DNMT3A-Mutated AML
Authors: Tomasz Rzymski, Urszula Pakulska, Camille Abboud, Howard A. Burris, Scott R. Solomon, Marta Obacz, Kristina Goller, Michal Combik, Jan Zaucha, Milena Mazan, Michal Mikula, Magdalena Cybulska, Anna Polak, Przemyslaw Juszczynski, Marcus Järås, Marion Chapellier, Johan Flygare, Magdalena Zawadzka, Karolina Bukowska Strakova, Krzysztof Brzozka, Setareh Shamsili, Noemi Angelosanto
Journal: Blood (2021)
Efficacy Analysis of Different FLT3 Inhibitors in Relapsed/Refractory Acute Myeloid Leukemia and High-Risk Myelodysplastic Syndrome Patients - a Systematic Review and Meta-Analysis
Authors: Mahesh Swaminathan, Mai M M Aly, Katherine G. Akers, Seongho Kim, Harry Ramos, Jaroslaw P. Maciejewski, Suresh Kumar Balasubramanian
Journal: Blood (2021)
Efficacy of HMA +/- Venetoclax or Intensive Chemotherapy in Blast-Phase Myeloproliferative Neoplasms
Authors: James J. Yoon, Lydia L. Benitez, Dale L. Bixby, Patrick W. Burke, Bernard L. Marini, Anthony J. Perissinotti, Moshe Talpaz, Kristen M. Pettit
Journal: Blood (2021)
Hypoxia-primed monocytes/macrophages enhance postinfarction myocardial repair
Authors: Yu Zhu, Wenjuan Yang, Hailong Wang, Fuqin Tang, Yun Zhu, Qiong Zhu, Ruiyan Ma, Zhao Jian, Yingbin Xiao
Journal: Theranostics (2021)

Background: Oxygen supplementation in myocardial infarction (MI) remains controversial. Inflammation is widely believed to play a central role in myocardial repair. A better understanding of these processes may lead to the design of novel strategies complementary to MI treatment. Methods: To investigate the role of hypoxia in inflammation and myocardial repair after acute MI, we placed MI mice in a tolerable mild hypoxia (10% O2) chamber for 7 days and then transferred the mice to ambient air for another 3 weeks. Results: We found that the cumulative survival rate of the MI mice under hypoxia was significantly higher than that under oxygen supplementation. Hypoxia promoted postinfarction myocardial repair. Importantly, we found that hypoxia modulated the phenotypic transition of blood monocytes from pro-inflammatory to pro-reparative in a timely manner, leading to the subsequent discontinuation of inflammation in myocardial tissues and promotion of myocardial repair post-MI. Specifically, cultured bone marrow-derived macrophages (BMDMs) primed by hypoxia in vitro exhibited improved reparative capacities and differed from M1 and M2 macrophages through the AMPKα2 signaling pathway. The deletion of AMPKα2 in monocytes/macrophages prevented the phenotypic transition induced by hypoxia and could not promote myocardial repair after MI when transplanted into the myocardium. Conclusions: Taken together, our work demonstrates that hypoxia promotes postinfarction myocardial repair by modulating the blood monocyte/macrophage phenotypic transition from pro-inflammatory to pro-reparative in a timely manner through the AMPKα2 signaling pathway. Hypoxia priming might be an attractive translational strategy for MI treatment by amplifying immune cells during early inflammation and subsequent resolution and repair.
Abstract 9331: Adverse Maternal Fetal Environment Partially Mediates Disparate Outcomes in Hispanic and Non Hispanic Black Infants With Critical Congenital Heart Disease
Authors: Stephanie Santana, Shabnam Peyvandi, John M Costello, Rebecca J Baer, James Collins, Tonia Branche, Laura Jelliffe-Pawlowski, Martina A Steurer
Journal: Circulation (2021)

Introduction: Etiologies of racial and ethnic disparities in critical congenital heart disease (CCHD) outcomes are not fully understood. We sought to determine whether differential exposure to an adverse maternal fetal environment (AMFE) partially explains disparate outcomes. Methods: We included infants with CCHD in a population-based administrative California database (2011-2017). Primary exposure was race/ethnicity. Primary mediator was AMFE, defined as maternal metabolic syndrome (MMS: any diabetes, abnormal BMI, or hyperlipidemia) or maternal placental syndrome (MPS: pre-eclampsia/ eclampsia, gestational hypertension, or placental abruption). Outcomes: days alive out of hospital in first year of life (DAOOH); composite of 1-year mortality or severe morbidity (e.g., ECMO, cardiac arrest, BPD, etc.). Mediation analyses (CCHD severity-adjusted) determined % contribution to outcome for each mediator on pathways between race/ethnicity and outcomes. Results: Included were 2,747 Non-Hispanic (NH) White [REF group], 5,244 Hispanic, and 625 NH Black infants. Hispanic and NH Black infants had higher risk for composite outcome (crude OR, 1.18; crude OR, 1.25 respectively) and fewer DAOOH (-6 &amp; -12 days, respectively). Relative to NH White infants (MMS 28%; MPS 12%), Hispanic infants had higher MMS exposure (43%, OR, 1.89), while NH Black infants had higher MMS (44%, OR, 1.97) &amp; MPS exposure (18%, OR, 1.66). Both MMS exposure (OR, 1.21) and MPS exposure (OR 1.56) were related to composite outcome and fewer DAOOH (-25 &amp; -16 days, respectively). AMFE explained 25% of relationship between NH Black race and composite outcome, and 18% of relationship between Hispanic ethnicity and composite outcome. AMFE explained 16% (NH Black race) and 21% (Hispanic ethnicity) of the association with DAOOH (Table). Conclusions: Increased exposure to AMFE contributes to disparate outcomes in NH Black and Hispanic infants with CCHD. This novel finding merits clinical attention.
Ten Year Follow up of the MD Anderson Cancer Center Phase 2 Study of Rituximab in Combination with Lenalidomide (R2) for Patients with Low Tumor Burden Follicular Lymphoma
Authors: Dai Chihara, Loretta Nastoupil, Paolo Strati, Felipe Samaniego, Lei Feng, Maria Alma Rodriguez, Luis Fayad, Jason R. Westin, Fredrick B. Hagemeister, Michael Wang, Sattva S. Neelapu, Nathan H. Fowler
Journal: Blood (2021)
Ocular Toxicity of Commercially Available Belantamab Mafodotin in Patients with Advanced Multiple Myeloma
Authors: Jithma P. Abeykoon, Luliana Vaxman, Sanjay V Patel, Shaji Kumar, Kimberly S Young, Sikander Ailawadhi, Jeremy T. Larsen, Wilson I Gonsalves, Taxiarchis Kourelis, Nelson Leung, Rahma M Warsame, Miriam A. Hobbs, Amie Fonder, Yi L. Hwa, P. Leif Bergsagel, Martha Q. Lacy, S. Vincent Rajkumar, Morie A. Gertz, Prashant Kapoor
Journal: Blood (2021)
Whole Genome Sequencing Identifies a Recurrent Mutation in Complement Factor I (<i>CFI</i>) in Primary Myelofibrosis (PMF)
Authors: Brooke Sadler, Anna D Chorzalska, Dennis M Bonal, Gabe Haller, Alissa Oakes, Max Petersen, Yuchen Liu, Adam Olszewski, John L Reagan, Pamela C Egan, Rabin Niroula, Diana O Treaba, Gabriela Hobbs, Stephen T. Oh, Jorge Di Paola, Joanna E Baxter, Patrycja M Dubielecka
Journal: Blood (2021)
Dichotomous effects of cellular expression of STAT3 on tumor growth of HNSCC
Authors: Thomas E. Bickett, Michael W. Knitz, Miles Piper, Ayman J. Oweida, Jacob Gadwa, Laurel B. Darragh, Diemmy Nguyen, Shilpa Bhatia, Shiv Bhuvane, Andy V. Phan, Benjamin Van Court, Sophia Corbo, Tiffany Pham, Alexander L. Dent, Laurel Lenz, Sana D. Karam
Journal: Molecular Therapy (2021)

STAT3 signaling has been shown to regulate cellular function and cytokine production in the tumor microenvironment (TME). Within the head and neck squamous cell carcinoma (HNSCC) TME, we previously showed that therapeutic targeting of STAT3 in combination with radiation resulted in improved tumor growth delay. However, given the independent regulatory effects STAT3 has on anti-tumor immunity, we aimed to decipher the effects of individually targeting STAT3 in the cancer cell, regulatory T cells (Tregs), and natural killer (NK) cell compartments in driving tumor growth and resistance to therapy in HNSCCs. We utilized a CRISPR knockout system for genetic deletion of STAT3 within the cancer cell as well as two genetic knockout mouse models, FoxP3-Cre/STAT3 fl and NKp46-Cre/STAT3 fl, for Tregs and NK cell targeting, respectively. Our data revealed differences in development of resistance to treatment with STAT3 CRISPR knockout in the cancer cell, driven by differential recruitment of immune cells. Knockout of STAT3 in Tregs overcomes this resistance and results in Treg reprogramming and recruitment and activation of antigen-presenting cells. In contrast, knockout of STAT3 in the NK cell compartment results in NK cell inactivation and acceleration of tumor growth. These data underscore the complex interplay between the cancer cell and the immune TME and carry significant implications for drug targeting and design of combination approaches in HNSCCs.
Abstract 10202: Ethnic/Racial Differences in Comorbidities and Outcome Among Patients with Amyloidosis: An Analysis of the National Inpatient Sample Database
Authors: Sarah Ream, Jennifer Ma, Tayana Rodriguez, Alejandro Sarabia-Gonzalez, Luis Alvarado, Alok Dwivedi, Debabrata Mukherjee
Journal: Circulation (2021)

Background: Amyloidosis is due to an abnormal extracellular deposition of insoluble fibrils in tissues. Prior studies have evaluated age and gender differences with amyloidosis, but there are no studies on racial/ethnic differences in risk factors and outcomes. We evaluate prevalence, characteristics, and outcomes in patients with amyloidosis across ethnic/racial groups. Methods: We performed a retrospective study utilizing the Nationwide Inpatient Sample (NIS) database from 2015 to 2018 using ICD-10 codes. We assessed demographics including age, race, gender and comorbidities including diabetes, hypertension, heart failure, pulmonary disease, coronary artery disease and renal failure according to ethnic/racial groups. Primary outcome was mortality. Unadjusted and adjusted relative risks (RR) with 95% confidence interval (CI) were calculated using survey weighted regression analysis. Results: Of the total population, amyloidosis prevalence was 0.17% (N=34,894). Blacks (RR 1.7, 95% CI 1.65-1.75, P &lt;.0001) and Hispanics (RR 1.27, 95% CI 1.22-1.33, P &lt;.0001) were more likely to be admitted to the hospital with amyloidosis compared to Whites. However, mortality was significantly higher among Whites while renal failure was higher in Blacks and Hispanics (P &lt;.0001). Conclusion: Our study suggests significant ethnic/racial differences in baseline characteristics and outcomes for hospitalized patients with amyloidosis. Mortality was significantly higher in White patients as compared to Blacks and Hispanics although Whites were significantly older and had more comorbidities. Additional studies are indicated to better understand differences in outcomes across ethnic/racial groups and the higher mortality in white individuals.
Role of the Inflammasome in Liver Disease
Authors: Marcelle de Carvalho Ribeiro, Gyongyi Szabo
Journal: Annual Review of Pathology Mechanisms of Disease (2021)

The involvement of inflammasomes in the proinflammatory response observed in chronic liver diseases, such as alcohol-associated liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD), is widely recognized. Although there are different types of inflammasomes, most studies to date have given attention to NLRP3 (nucleotide-binding oligomerization domain-like receptor family, pyrin domain containing 3) in the pathogenesis of ALD, NAFLD/nonalcoholic steatohepatitis, and fibrosis. Canonical inflammasomes are intracellular multiprotein complexes that are assembled after the sensing of danger signals and activate caspase-1, which matures interleukin (IL)-1β, IL-18, and IL-37 and also induces a form of cell death called pyroptosis. Noncanonical inflammasomes activate caspase-11 to induce pyroptosis. We discuss the different types of inflammasomes involved in liver diseases with a focus on (a) signals and mechanisms of inflammasome activation, (b) the role of different types of inflammasomes and their products in the pathogenesis of liver diseases, and (c) potential therapeutic strategies targeting components of the inflammasomes or cytokines produced upon inflammasome activation.
Association of Sodium-Glucose Transport Protein 2 Inhibitor Use for Type 2 Diabetes and Incidence of Gout in Taiwan
Authors: Mu-Chi Chung, Peir-Haur Hung, Po-Jen Hsiao, Laing-You Wu, Chao-Hsiang Chang, Ming-Ju Wu, Jeng-Jer Shieh, Chi-Jung Chung
Journal: JAMA Network Open (2021)

<h3>Importance</h3> The use of sodium-glucose transport protein 2 (SGLT2) inhibitors is currently a standard intervention in patients with type 2 diabetes (T2DM) and exerts favorable pleiotropic effects to consistently lower blood urate levels. However, to date, no association between SGLT2 inhibitor use and the incidence of gout have been established. <h3>Objective</h3> To investigate whether prescribed SGLT2 inhibitors are associated with lower gout incidence in patients with T2DM. <h3>Design, Setting, and Participants</h3> In a cohort study, all patients with incident T2DM in Taiwan National Health Institution databases between May 1, 2016, and December 31, 2018, were retrospectively analyzed. As a comparator, patients using dipeptidyl peptidase 4 (DPP4) inhibitors were included. A total of 47 905 individuals receiving an SGLT2 inhibitor and 183 303 receiving a DPP4 inhibitor were evaluated, along with 47 405 pairs of patients using an SGLT2 inhibitor or DPP4 inhibitor in 1:1 propensity score–matched analyses. Data analysis was conducted from April 1 to June 30, 2021. <h3>Main Outcomes and Measures</h3> A gout diagnosis was based on the<i> International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM)</i>and the<i>International Statistical Classification of Diseases, Tenth Revision, Clinical Modification (ICD-10-CM).</i>Multiple Cox proportional hazards regression models were used to calculate hazard ratios (HRs) and 95% CIs. <h3>Results</h3> In total, 231 208 patients with T2DM were included in the population; 113 812 individuals (49.22%) were women, and the mean (SD) age was 61.53 (12.86) years. The overall gout incidence was 20.26 per 1000 patient-years for SGLT2 inhibitor users and 24.30 per 1000 patient-years for DPP4 inhibitor users. When potential risk factors were adjusted in the propensity score–matched population, use of SGLT2 inhibitors was associated with a lower risk of gout (HR, 0.89; 95% CI, 0.82-0.96) compared with DPP4 inhibitors, particularly for patients receiving dapagliflozin (HR, 0.86; 95% CI, 0.78-0.95). A sensitivity analysis, performed when a gout diagnosis was ascertained using the<i>ICD-9-CM</i>or<i>ICD-10-CM</i>code with gout-related medication, also showed a significantly lower risk for gout incidence of 15% with SGLT2 inhibitors (HR, 0.85; 95% CI, 0.74-0.97). Subgroup analysis indicated that SGLT2 inhibitor benefits in patients with T2DM to achieve a lower gout risk were not different across subgroups. <h3>Conclusions and Relevance</h3> The findings of this study suggest that patients with T2DM who are receiving SGLT2 inhibitors may have a lower risk for gout compared with those receiving DPP4 inhibitors.
ALPHA Study: ALLO-501 Produced Deep and Durable Responses in Patients with Relapsed/Refractory Non-Hodgkin's Lymphoma Comparable to Autologous CAR T
Authors: Sattva S. Neelapu, Rajneesh Nath, Javier Munoz, Michael Tees, David B. Miklos, Matthew J. Frank, Shahbaz A. Malik, Don Stevens, Chu Ri Shin, Arun Balakumaran, Lynn Loomis-Navale, Lovely Goyal, Anh Nguyen, Frederick L. Locke
Journal: Blood (2021)
A Randomized Placebo-Controlled Phase 2 Study of Metformin for the Prevention of Progression of Monoclonal Gammopathy of Undetermined Significance and Low Risk Smoldering Multiple Myeloma
Authors: Catherine R. Marinac, Robert A. Redd, Julia Prescott, Alexandra Savell, Courtney Igne, Jacob P. Laubach, Adam S. Sperling, Aric D. Parnes, Houry Leblebjian, Paul G. Richardson, Irene M. Ghobrial, Omar Nadeem
Journal: Blood (2021)
Effect of the COVID-19 Pandemic on Adolescents With Eating Disorders—Reply
Authors: Nicole Racine, Tracy Vaillancourt, Sheri Madigan
Journal: JAMA Pediatrics (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 Pediatrics HomeNew OnlineCurrent IssueFor Authors Podcast Journals 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 2024 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 Pediatrics journal
Tumor-infiltrating lymphocytes are functionally inactivated by CD90+ stromal cells and reactivated by combined Ibrutinib and Rapamycin in human pleural mesothelioma
Authors: Haitang Yang, Sabina Berezowska, Patrick Dorn, Philipp Zens, Peiru Chen, Ren-Wang Peng, Thomas M. Marti, Gregor J Kocher, Ralph A. Schmid, Sean R.R. Hall
Journal: Theranostics (2021)

Rationale: Despite evidence suggesting that the tumor microenvironment (TME) in malignant pleural mesothelioma (MPM) is linked with poor prognosis, there is a lack of studies that functionally characterize stromal cells and tumor-infiltrating lymphocytes (TILs). Here, we aim to characterize the stromal subsets within MPM, investigate their relationship to TILs, and explore the potential therapeutic targets. Methods: We curated a core set of genes defining stromal/immune signatures expressed by mesenchymal cells within the TME using molecular analysis of The Cancer Genome Atlas (TCGA) MPM cohort. Stromal and immune profiles were molecularly characterized using flow cytometry, immunohistochemistry, microarray, and functionally evaluated using T cell-activation/expansion, coculture assays and drug compounds treatment, based on samples from an independent MPM cohort. Results: We found that a high extracellular matrix (ECM)/stromal gene signature, a high ECM score, or the ratio of ECM to an immune activation gene signature are significantly associated with poor survival in the MPM cohort in TCGA. Analysis of an independent MPM cohort (n = 12) revealed that CD8+ and CD4+ TILs were characterized by PD1 overexpression and concomitant downregulation in degranulation and CD127. This coincided with an increase in CD90+ cells that overexpressed PD-L1 and were enriched for ECM/stromal genes, activated PI3K-mTOR signaling and suppressed T cells. Protein array data demonstrated that MPM samples with high PD-L1 expression were most associated with activation of the mTOR pathway. Further, to reactivate functionally indolent TILs, we reprogrammed ex vivo TILs with Ibrutinib plus Rapamycin to block interleukin-2-inducible kinase (ITK) and mTOR pathways, respectively. The combination treatment shifted effector memory (TEM) CD8+ and CD4+ TILs towards T cells that re-expressed CD45RA (TEMRA) while concomitantly downregulating exhaustion markers. Gene expression analysis confirmed that Ibrutinib plus Rapamycin downregulated coinhibitory and T cell signature pathways while upregulating pathways involved in DNA damage and repair and immune cell adhesion and migration. Conclusions: Our results suggest that targeting the TME may represent a novel strategy to redirect the fate of endogenous TILs with the goal of restoring anti-tumor immunity and control of tumor growth in MPM.
The Sumoylation Inhibitor TAK-981 in Combination with the CD19-Targeting Antibody Tafasitamab Shows Enhanced Anti-Tumor Activity in Preclinical B-Cell Lymphoma Models
Authors: Maria Patra-Kneuer, Akito Nakamura, Keli Song, Stephen Grossman, Andrea Polzer, Carmen Ginzel, Stefan Steidl, Allison J Berger, Igor Proscurshim, Christina Heitmüller
Journal: Blood (2021)
S1P/S1PR1 Signalis Required for Optimal T-Cell Pathogenicity to Induce Gvhd By RegulatingDrp1/mTOR Axis
Authors: Linlu Tian, Yongxia Wu, Hee-Jin Choi, Xiaohui Sui, Mohammed Hanief Sofi, Mohamed Faisal Kassir, Paul J Martin, Shikhar Mehrotra, Besim Ogretmen, Xue-Zhong Yu
Journal: Blood (2021)
SERF1 Is Required for G-CSF Resistance of Start-Codon Mutant <i>ELANE</i> Granulocytic Precursors
Authors: Ramesh C Nayak, Lisa Trump, Sana Emberesh, Yarim Lee, Abhishek K Singh, Ashley M Wellendorf, Marshall S. Horwitz, Theodosia A. Kalfa, Carolyn Lutzko, Jose A. Cancelas
Journal: Blood (2021)
Efficacy of Cobimetinib in Rosai-Dorfman Disease
Authors: Jithma P. Abeykoon, Karen Rech, Aishwarya Ravindran, Aldo A. Acosta-Medina, Saurabh Zanwar, Jason R. Young, W. Oliver Tobin, Mithun V. Shah, Nora Bennani, Robert Vassallo, Jay Ryu, Matthew Koster, Caroline J Davidge-Pitts, Gaurav Goyal, Ronald Go
Journal: Blood (2021)
Clinically Relevant Circulating Protein Biomarkers for Type 1 Diabetes: Evidence From a Two-Sample Mendelian Randomization Study
Authors: Nahid Yazdanpanah, Mojgan Yazdanpanah, Ye Wang, Vincenzo Forgetta, Michael Pollak, Constantin Polychronakos, J. Brent Richards, Despoina Manousaki
Journal: Diabetes Care (2021)

OBJECTIVE To identify circulating proteins influencing type 1 diabetes susceptibility using Mendelian randomization (MR). RESEARCH DESIGN AND METHODS We used a large-scale two-sample MR study, using cis genetic determinants (protein quantitative trait loci [pQTL]) of up to 1,611 circulating proteins from five large genome-wide association studies, to screen for causal associations of these proteins with type 1 diabetes risk in 9,684 case subjects with type 1 diabetes and 15,743 control subjects. Further, pleiotropy-robust MR methods were used in sensitivity analyses using both cis and trans-pQTL. RESULTS We found that a genetically predicted SD increase in signal regulatory protein gamma (SIRPG) level was associated with increased risk of type 1 diabetes risk (MR odds ratio [OR] 1.66 [95% 1.36–2.03]; P = 7.1 × 10−7). The risk of type 1 diabetes increased almost twofold per genetically predicted standard deviation (SD) increase in interleukin-27 Epstein-Barr virus–induced 3 (IL27-EBI3) protein levels (MR OR 1.97 [95% CI 1.48–2.62]; P = 3.7 × 10−6). However, an SD increase in chymotrypsinogen B1 (CTRB1) was associated with decreased risk of type 1 diabetes (MR OR 0.84 [95% CI 0.77–0.90]; P = 6.1 × 10−6). Sensitivity analyses using MR methods testing for pleiotropy while including trans-pQTL showed similar results. While the MR-Egger suggested no pleotropic effect (P value MR-Egger intercept = 0.31), there was evidence of pleiotropy in MR-PRESSO (P value global test = 0.006). CONCLUSIONS We identified three novel circulating protein biomarkers associated with type 1 diabetes risk using an MR approach. These biomarkers are promising targets for development of drugs and/or of screening tools for early prediction of type 1 diabetes.
A Phase I Clinical Trial Testing the Safety of IL-21-Expanded, Universally Alloreactive Donor-Derived Natural Killer Cells for Relapsed/Refractory Acute Myeloid Leukemia and Myelodysplastic Syndrome
Authors: Sumithira Vasu, Nidhi Sharma, Alison R. Walker, Sarah A Wall, James S. Blachly, Greg K. Behbehani, Hannah Choe, Aarohi Thakkar, Robin Nakkula, Ella Troy, Nicole Szuminski, Marcos J.G. de Lima, Lynn O'Donnell, Dean Anthony Lee
Journal: Blood (2021)