tbuckley/cabot-search huggingface dataset:
Abstract #2061: Green tea health benefits and costs_It's about finding balance
Authors: Jordan McDonald, J. McBride, A. Garrett, J. Handy, R. Enz, B. Murray, R. Robison, K. O'Neill
Journal: Cancer Research (2009)

Green tea is a known chemopreventive agent that has the beneficial effects of inhibiting metastasis and cancer progression. It also inhibits angiogenesis, which is necessary for tumor growth. Additionally, green tea has even found use as a weight loss supplement. On the other hand, green tea is found to be hepatotoxic and shown to inhibit open wound healing at high concentrations. This study seeks to understand the balance between the benefits and the deleterious effects of green tea. Green tea contains beneficial flavonoids that act as strong antioxidants. Using the Oxygen Radical Absorbance Capacity (ORAC) Assay, which measures the ability of a substance to prevent oxidation of a fluorescent species, we found that green tea has a Trolox equivalent (TE) of 2120 umol Trolox/uL whole green tea. Black tea and white tea were measured at 2108 and 2106 TE, respectively (Trolox ® = 6-Hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic Acid). We also treated human Burkitt\#8217;s lymphoma cells with green tea, black tea, and white tea in a 1:10 dilution. The results demonstrated an inhibition of cell growth by 43%, 40%, and 32%, respectively. Further research is ongoing to determine the effect on immune function of the respective teas. It has been suggested that a constituent of green tea, epigallocatechin gallate (EGCG), is one of the most potent antioxidant species found in green tea. Indeed, analysis with the ORAC Assay demonstrates that EGCG accounts for 50% of the antioxidant capacity of whole green tea, having an ORAC value of 13,700 umol Trolox ®/g of EGCG in solution. However, using a modified Alkaline Comet Assay that accurately measures DNA damage, our research shows that treatment of naked Jurkat cell DNA treated for 120 minutes with a physiological concentration of EGCG of 0.3 uM causes DNA damage. The Comet Assay resulted in a tail profile of greater than .20 compared to the untreated control cells that had a tail profile of 0.05. The tail profile is the ratio between the tail intensity and the total comet intensity; the larger the tail intensity the greater the DNA damage and the closer the ratio moves to one. Our data confirms results found by Johnson and Loo (2000), who showed that high concentrations of EGCG damage DNA of Jurkat cells treated whole at a concentration of 100 uM EGCG. This suggests that naked DNA is highly sensitive to damage by EGCG. These results confirm previous findings and suggest a mechanism whereby the components of green tea, namely EGCG, can cause DNA damage, thus leading to increased mutation rates and ultimately cancer. We conclude that green tea is best if taken in moderation. Low concentrations are shown to be highly beneficial, however, if ingested in large or concentrated amounts green tea can do more harm than benefit.  Citation Information: In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 2061.
Real-World Clinical Management of Patients with Congenital Hemophilia and Inhibitors: Interim Analysis of the FEIBA Global Outcome Study (FEIBA GO)
Authors: Cedric Hermans, Claude Négrier, Pål A Holme, Carmen Escuriola, Ana R Cid, Nataliya Kemenyash, Jaco Botha, Viridiana Cano-Garcia, Jerzy Windyga
Journal: Blood (2020)
Multiomics profiling of primary lung cancers and distant metastases reveals immunosuppression as a common characteristic of tumor cells with metastatic plasticity
Authors: Won-Chul Lee, Alexandre Reuben, Xin Hu, Nicholas McGranahan, Runzhe Chen, Ali Jalali, Marcelo V. Negrao, Shawna M. Hubert, Chad Tang, Chia-Chin Wu, Anthony San Lucas, Whijae Roh, Kenichi Suda, Jihye Kim, Aik-Choon Tan, David H. Peng, Wei Lu, Ximing Tang, Chi-Wan Chow, Junya Fujimoto, Carmen Behrens, Neda Kalhor, Kazutaka Fukumura, Marcus Coyle, Rebecca Thornton, Curtis Gumbs, Jun Li, Chang-Jiun Wu, Latasha Little, Emily Roarty, Xingzhi Song, J. Jack Lee, Erik P. Sulman, Ganesh Rao, Stephen Swisher, Lixia Diao, Jing Wang, John V. Heymach, Jason T. Huse, Paul Scheet, Ignacio I. Wistuba, Don L. Gibbons, P. Andrew Futreal, Jianhua Zhang, Daniel Gomez, Jianjun Zhang
Journal: Genome biology (2020)

Abstract Background Metastasis is the primary cause of cancer mortality accounting for 90% of cancer deaths. Our understanding of the molecular mechanisms driving metastasis is rudimentary. Results We perform whole exome sequencing (WES), RNA sequencing, methylation microarray, and immunohistochemistry (IHC) on 8 pairs of non-small cell lung cancer (NSCLC) primary tumors and matched distant metastases. Furthermore, we analyze published WES data from 35 primary NSCLC and metastasis pairs, and transcriptomic data from 4 autopsy cases with metastatic NSCLC and one metastatic lung cancer mouse model. The majority of somatic mutations are shared between primary tumors and paired distant metastases although mutational signatures suggest different mutagenesis processes in play before and after metastatic spread. Subclonal analysis reveals evidence of monoclonal seeding in 41 of 42 patients. Pathway analysis of transcriptomic data reveals that downregulated pathways in metastases are mainly immune-related. Further deconvolution analysis reveals significantly lower infiltration of various immune cell types in metastases with the exception of CD4+ T cells and M2 macrophages. These results are in line with lower densities of immune cells and higher CD4/CD8 ratios in metastases shown by IHC. Analysis of transcriptomic data from autopsy cases and animal models confirms that immunosuppression is also present in extracranial metastases. Significantly higher somatic copy number aberration and allelic imbalance burdens are identified in metastases. Conclusions Metastasis is a molecularly late event, and immunosuppression driven by different molecular events, including somatic copy number aberration, may be a common characteristic of tumors with metastatic plasticity.
Bruton's Tyrosine Kinase Inhibitors Impair Fcγriia-Mediated Responses of Healthy Donor Platelets and Chronic Lymphocytic Leukaemia Derived Platelets to Bacteria
Authors: Leigh Naylor-Adamson, Zoe Booth, Simon Hart, Russell Patmore, Sujoy Khan, David Allsup, Monica Arman
Journal: Blood (2020)
Hemocompatibility-Related Adverse Events and Survival on Venoarterial Extracorporeal Life Support
Authors: Mabel Chung, Fausto R Cabezas, Jose I Nunez, Kevin F Kennedy, Katelyn Rick, Peter Rycus, Mandeep R Mehra, A Reshad Garan, Robb D Kociol, E Wilson Grandin
Journal: JACC Heart Failure (2020)
One-Year Follow-up of ZUMA-2, the Multicenter, Registrational Study of KTE-X19 in Patients with Relapsed/Refractory Mantle Cell Lymphoma
Authors: Michael Wang, Javier Munoz, Andre H. Goy, Frederick L. Locke, Caron A. Jacobson, Brian T. Hill, John M. Timmerman, Houston Holmes, Samantha Jaglowski, Ian W. Flinn, Peter A. McSweeney, David B. Miklos, John M. Pagel, Marie José Kersten, Noel Milpied, Henry C.H. Fung, Max S. Topp, Roch Houot, Amer Beitinjaneh, Weimin Peng, Lianqing Zheng, John M. Rossi, Swaminathan Murugappan, Ioana Kloos, Patrick M. Reagan
Journal: Blood (2020)
Patterns of Tocilizumab Use Among Myeloma Patients Receiving Bcma-Directed Therapies: Effect on Day 30 Outcomes
Authors: Jeffrey Marsal, Rahul Banerjee, Chiung-Yu Huang, Mimi Lo, Vanessa E Kennedy, Shagun Arora, Jeffrey L. Wolf, Thomas Martin, Sandy W. Wong, Nina Shah
Journal: Blood (2020)
Real-World Treatment of Pediatric Patients with Relapsed/Refractory B-Cell Acute Lymphoblastic Leukemia Using Tisagenlecleucel That Is out of Specification for Commercial Release
Authors: Jenna Rossoff, Christina Baggott, Snehit Prabhu, Holly Pacenta, Christine L Phillips, Heather Stefanski, Julie-An Talano, Amy Moskop, Steven P. Margossian, Michael R Verneris, Gary Douglas Myers, Nicole Karras, Patrick A. Brown, Muna Qayed, Michelle Hermiston, Prakash Satwani, Christa Krupski, Amy Keating, Rachel Wilcox, Cara A Rabik, Vanessa Fabrizio, Michael Kunicki, Vasant Chinnabhandar, A. Yasemin Goksenin, Kevin J. Curran, Crystal L. Mackall, Theodore W. Laetsch, Liora M. Schultz
Journal: Blood (2020)
Reshaping the Immune Microenvironment by Oncolytic Herpes Simplex Virus in Murine Pancreatic Ductal Adenocarcinoma
Authors: Liming Zhang, Wei Wang, Ruikun Wang, Nianchao Zhang, Hang Shang, Yang Bi, Da Chen, Cuizhu Zhang, Long Li, Jie Yin, Hongkai Zhang, Youjia Cao
Journal: Molecular Therapy (2020)

Pancreatic ductal adenocarcinoma (PDAC) is the major type of pancreatic malignancy with very poor prognosis. Despite the promising results of immune checkpoint inhibitors (ICIs) in some solid tumors, immunotherapy is less effective for PDAC due to its immunosuppressive tumor microenvironment (TME). In this report, we established an immunocompetent syngeneic PDAC model and investigated the effect of oncolytic herpes simplex virus-1 (oHSV) on the composition of TME immune cells. The oHSV treatment significantly reduced tumor burden and prolonged the survival of tumor-bearing mice. Further, by single cell RNA sequencing (scRNA-seq) and multicolor fluorescence-activated cell sorting (FACS) analysis, we demonstrated that oHSV administration downregulated tumor-associated macrophages (TAMs), especially the anti-inflammatory macrophages, and increased the percentage of tumor-infiltrating lymphocytes, including activated cytotoxic CD8+ T cells and T helper (Th)1 cells. Besides, the combination of oHSV and immune checkpoint modulators extended the lifespan of the tumor-bearing mice. Overall, our data suggested that oHSV reshapes the TME of PDAC by boosting the immune activity and leads to improved responsiveness of PDAC to immunotherapy.
Hypoxic Glioma Stem Cell–Derived Exosomes Containing Linc01060 Promote Progression of Glioma by Regulating the MZF1/c-Myc/HIF1α Axis
Authors: Junjun Li, Tingting Liao, Hongya Liu, Hongliang Yuan, Taohui Ouyang, Jiajing Wang, Songshan Chai, Jinsong Li, Jingchao Chen, Xiang Li, Hongyang Zhao, Nanxiang Xiong
Journal: Cancer Research (2020)

Glioma stem cells (GSC) are a subpopulation of tumor cells with special abilities to proliferate and differentiate in gliomas. They are one of the main causes of tumor recurrence, especially under hypoxic conditions. Although long noncoding RNAs (lncRNA) are known to be involved in numerous biological processes and are implied in the occurrence of certain diseases, their role in tumor development and progression remains poorly understood. Here we explored the mechanisms by which lncRNA derived from hypoxic GSCs (H-GSC) cause glioma progression. Isolation and identification of the Linc01060 gene, the exosomes containing them, and the proteins from tumor cells regulating the gene allowed for studying the effects of Linc01060 on proliferation and glycometabolism. H-GSC exerted their effects by transferring exosomes to glioma cells, resulting in a significant increase in Linc01060 levels. Mechanistically, Linc01060 directly interacted with the transcription factor myeloid zinc finger 1 (MZF1) and enhanced its stability. Linc01060 facilitated nuclear translocation of MZF1 and promoted MZF1-mediated c-Myc transcriptional activities. In addition, c-Myc enhanced the accumulation of the hypoxia-inducible factor-1 alpha (HIF1α) at the posttranscriptional level. HIF1α bound the hormone response elements of the Linc01060 promoter, upregulating the transcription of Linc01060 gene. Clinically, Linc01060 was upregulated in glioma and was significantly correlated with tumor grade and poor clinical prognosis. Overall, these data show that secretion of Linc01060-containing exosomes from H-GSCs activates prooncogenic signaling pathways in glioma cells to promote disease progression. SIGNIFICANCE: These findings suggest that inhibition of Linc01060-containing exosomes or targeting the Linc01060/MZF1/c-Myc/HIF1α axis may be an effective therapeutic strategy in glioma.
Efficacy and Safety of Amlodipine in Preventing Myocardial Iron Overload in Patients with Transfusion-Dependent Thalassemia Major : A Systematic Review and Meta-Analysis
Authors: Richi Kashyap, Muhammad Ashar Ali, Saad Ullah Malik, Farhan Khalid, Ali Jaan, Awais Khalid, Abdul Jabbar Dar, Qasim Khurshid, Karun Neupane, Mobeen Zaka Haider, Syed Maaz Abdullah, Faiz Anwer
Journal: Blood (2020)
Abstract 409: Investigating the Role of the Mitochondrial Calcium Uniporter (mcu) in Calcium Regulation of Cardiac Mitochondria Using Transmural Spectroscopy and an Integrating Sphere
Authors: Anna Kosmach, Junhui Sun, Armel Femnou, Robert S Balaban, Elizabeth Murphy
Journal: Circulation Research (2020)

Cardiac mitochondria uptake calcium through the mitochondrial calcium uniporter (MCU). To better understand the role of MCU and mitochondrial calcium in regulating heart physiology and pathophysiology, we developed a method to measure mitochondrial matrix calcium in beating, perfused hearts. Langendorff perfusing hearts are loaded with 4.5 uM rhod-2-AM at 30°C and then perfused at 37°C to washout uncleaved dye. We determined that rhod-2 localized primarily to the mitochondria under our loading conditions, as shown by loading in a heart expressing a GFP-tagged mitochondrial outer membrane protein and analyzing heart slices under super resolution microscopy. Further, addition of Mn 2+ , which quenches cytosolic rhod-2, has little effect on rhod-2 signal. We insert an optical catheter with both white light and 532nm laser into the left ventricle and interleaved the collection of spectra from both light sources. The perfused heart is center mounted in an integrating sphere for spectra collection. The light passes through the ventricle and reflects off the integrating sphere resulting in a near uniform sampling of the transmitted light. Spectral properties from both light sources are determined using a rapid scanning spectrophotometer. Myoglobin oxygenation, cytochrome redox state, and rhod-2 loading are determined by white light absorbance. Ca 2+ bound rhod-2 emission is determined by removing background tissue effects from laser emission spectra and normalizing to tissue absorbance. Using this method we are able to measure changes in Ca 2+ and cytochromes during treatments such as isoproterenol and ischemia-reperfusion. The use of an integrating sphere transmural spectroscopy provides us an unique method to study mitochondrial Ca 2+ signaling in perfused mouse heart loaded with Rhod-2.
Maturation of the gut microbiome during the first year of life contributes to the protective farm effect on childhood asthma
Authors: Martin Depner, Diana Hazard Taft, Pirkka V. Kirjavainen, Karen M. Kalanetra, Anne M. Karvonen, Stefanie Peschel, Elisabeth Schmausser-Hechfellner, Caroline Roduit, Remo Frei, Roger Lauener, Amandine Divaret-Chauveau, Jean-Charles Dalphin, Josef Riedler, Marjut Roponen, Michael Kabesch, Harald Renz, Juha Pekkanen, Freda M. Farquharson, Petra Louis, David A. Mills, Erika von Mutius, Markus J. Ege
Journal: Nature Medicine (2020)
Targeting fibroblast growth factor 23-responsive pathways uncovers controlling genes in kidney mineral metabolism
Authors: Pu Ni, Erica L. Clinkenbeard, Megan L. Noonan, Joseph M. Richardville, Jeanette McClintick, Takashi Hato, Danielle Janosevic, Ying-Hua Cheng, Tarek M. El-Achkar, Michael T. Eadon, Pierre C. Dagher, Kenneth E. White
Journal: Kidney International (2020)
Pharmacodynamic Evaluation of Acalabrutinib in Relapsed/Refractory and Treatment-Naive Patients with Chronic Lymphocytic Leukemia (CLL) in the Phase 1/2 ACE-CL-001 Study
Authors: Todd Covey, Michael Gulranjani, Jean Cheung, Elena Bibikova, Tracy Clevenger, Fanny Krantz, Karen Pan, Kyoko Yamaguchi, Anouk De Jong, Bart Van Lith, Diana Mittag, Raquel Izumi, John C. Byrd, William G Wierda, Susan M. O'Brien, Richard R. Furman, Allard Kaptein
Journal: Blood (2017)
Sugary Drinks, Artificially-Sweetened Beverages, and Cardiovascular Disease in the NutriNet-Santé Cohort
Authors: Eloi Chazelas, Charlotte Debras, Bernard Srour, Léopold K. Fezeu, Chantal Julia, Serge Hercberg, Mélanie Deschasaux, Mathilde Touvier
Journal: Journal of the American College of Cardiology (2020)
Fine Mapping of the Major Histocompatibility Complex Region and Association of the HLA-B*52:01 Allele With Cervical Cancer in Japanese Women
Authors: Tatsuo Masuda, Hidemi Ito, Jun Hirata, Saori Sakaue, Yutaka Ueda, Tadashi Kimura, Fumihiko Takeuchi, Yoshinori Murakami, Koichi Matsuda, Keitaro Matsuo, Yukinori Okada
Journal: JAMA Network Open (2020)

<h3>Importance</h3> Understanding the genetic contribution of the major histocompatibility complex (MHC) region to the risk of cervical cancer (CC) will help understand how immune responses to infection with human papillomaviruses are associated with CC. <h3>Objective</h3> To determine whether the HLA-B*52:01 allele is associated with CC in Japanese women. <h3>Design, Setting, and Participants</h3> This was a multicenter genetic association study. Genotype and phenotype data were obtained from BioBank Japan Project. Additional patients with CC were enrolled from the Aichi Cancer Center Research Institute. An MHC fine-mapping study was conducted on CC risk in the Japanese population by applying a human leukocyte antigen (HLA) imputation method to the large-scale CC genome-wide association study data of using the Japanese population-specific HLA reference panel. Participants included 540 women in BioBank Japan Project with CC or 39 829 women without gynecologic diseases, malignant neoplasms, and MHC-related diseases as controls. An additional 168 patients with CC were recruited from Aichi Cancer Center Research Institute. Histopathological subtypes and clinical stages were not considered. Participants with low genotype call rate, closely related participants, and outliers in the principal component analysis were excluded. Data analysis was performed from August 2018 to January 2020. <h3>Main Outcomes and Measures</h3> Loci within the MHC region associated with CC risk, and the direction and size of association. <h3>Results</h3> A total of 704 CC cases and 39 556 controls were analyzed. All participants were Japanese women with a median (range) age of 67 (18 to 100) years. One of the class I HLA alleles of HLA-B*52:01 was significantly associated with CC risk (odds ratio, 1.60; 95% CI, 1.38-1.86;<i>P</i> = 7.4 × 10<sup>−10</sup>). Allele frequency spectra of HLA-B*52:01 are heterogeneous among worldwide populations with high frequency in Japanese populations (0.109 in controls), suggesting its population–specific risk associated with CC. The conditional analysis suggested that HLA-B*52:01 could explain most of the MHC risk associated with CC because no other HLA alleles remained significant after conditioning on the HLA-B*52:01. The HLA amino acid residue–based analysis suggested that HLA-B p.Tyr171His located in the peptide-binding groove was associated with the most significant CC risk (odds ratio, 1.47; 95% CI, 1.30-1.66;<i>P</i> = 1.2 × 10<sup>−9</sup>). <h3>Conclusions and Relevance</h3> The results of this study contribute to understanding of the genetic background of CC. The results suggest that immune responses mediated by class I HLA molecules are associated with susceptibility to CC.
The Impact of Ethnicity on the Response to Eltrombopag in Patients with Immune Thrombocytopenia (ITP) in Qatar: A Single Institution Experience
Authors: Mohamed A Yassin, Aya Alasmar, Rola Ghasoub, Omer Ismail, Abdulqadir Jeprel Nashwan, Firdous Ghori, Deena Sideeg, Radwa M Hussein, Randa Al -Okka, Prem Chandra, Anas Hamad, Ashraf Tawfiq Soliman
Journal: Blood (2020)
SAT0120 Psychological adjustment mediates the relationship of somatic symptoms with mental health and physical function in rheumatoid arthritis
Authors: GJ Treharne, AC Lyons, S Mason, S Macey, GD Kitas
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> Pain and fatigue have been linked to negative mental and physical outcome in Rheumatoid Arthritis (RA), but this link may be mediated by psychological processes. <h3>Objectives</h3> To examine whether the link of RA symptoms to well-being is mediated by the process of psychological adjustment, defined as Disease Self-Efficacy (belief in certain abilities), Disease Acceptance (the ability to accommodate disease-generated stressors), and General Self-Discrepancy (the distance between the actual and ideal self-concepts). <h3>Methods</h3> Patients:140 random, consenting hospital outpatients with RA. Instruments: (a) Somatic symptoms: Visual Analogue Scales for pain and fatigue; (b) Mental Health: Hospital Anxiety and Depression Scale (HAD); (c) Physical Function: Health Assessment Questionnaire (HAQ); (d) Psychological Adjustment: Arthritis Self-Efficacy Scale (ASES), Acceptance of Illness Scale (AIS), and Self-Discrepancy Scale (SDS). Statistics: correlation, hierarchical multiple regression. <h3>Results</h3> Regression strategies to detect mediators indicated that: Disease Acceptance and Self-Efficacy For Other Symptoms mediated the relationship between Fatigue and Depression (beta reducing from 0.28, p &lt; 0.01, to 0.02, n.s.); Self-Efficacy for Other Symptoms also mediated the relationship between Pain and Depression (beta reducing from 0.23, p &lt; 0.05, to 0.11, n.s.); and Self-Efficacy for Pain mediated the relationship between Pain and Physical Function (beta reducing from 0.21, p &lt; 0.05, to 0.08, n.s.). <h3>Conclusion</h3> Disease Acceptance and Self-Efficacy as measures of Psychological Adjustment mediate the relationship of somatic symptoms with mental health and physical function in RA. They may be appropriate targets for intervention in patients with RA.
Initial Treatment with Lenalidomide Plus Rituximab for Mantle Cell Lymphoma (MCL): 7-Year Analysis from a Multi-Center Phase II Study
Authors: Samuel Yamshon, Peter Martin, Bijal Shah, Stephen J. Schuster, Paul J Christos, Amelyn Rodriguez, Sonali M. Smith, Jakub Svoboda, Richard R. Furman, Sarah C. Rutherford, John N. Allan, John P. Leonard, Jia Ruan
Journal: Blood (2020)
Currently relevant p-phenylenediamine patch test reactions associated with hair dye and nonscalp anatomic areas: Retrospective cross-sectional analysis of North American Contact Dermatitis Group data, 2001 to 2016
Authors: Erin M. Warshaw, Sara A. Kullberg, Amber R. Atwater, Joel G. DeKoven, Jonathan I. Silverberg, Donald V. Belsito, Joseph F. Fowler, Anthony F. Fransway, Vincent A. DeLeo, Howard I. Maibach, Kathryn A. Zug, Margo J. Reeder, James S. Taylor, Denis Sasseville, Melanie D. Pratt
Journal: Journal of the American Academy of Dermatology (2020)
High Efficacy of Liposomal Annamycin (L-ANN) in Combination with Cytarabine in Syngeneic p53-Null AML Mouse Model
Authors: Tomasz Zal, Rafal Zielinski, Krzysztof Grela, Roberto Cardenas-Zuniga, Stanislaw Skora, Izabela Fokt, Malgorzata Anna Zal, Michael Andreeff, Lidia Gil, Robert Shephard, Waldemar Priebe
Journal: Blood (2020)
Embracing Change: Continual Learning in Deep Neural Networks
Authors: Raia Hadsell, Dushyant Rao, Andrei A. Rusu, Razvan Pascanu
Journal: Trends in Cognitive Sciences (2020)

Artificial intelligence research has seen enormous progress over the past few decades, but it predominantly relies on fixed datasets and stationary environments. Continual learning is an increasingly relevant area of study that asks how artificial systems might learn sequentially, as biological systems do, from a continuous stream of correlated data. In the present review, we relate continual learning to the learning dynamics of neural networks, highlighting the potential it has to considerably improve data efficiency. We further consider the many new biologically inspired approaches that have emerged in recent years, focusing on those that utilize regularization, modularity, memory, and meta-learning, and highlight some of the most promising and impactful directions.
Long-Term Follow-up of Ruxolitinib in Treatment of Steroid-Refractory Chronic Graft-Versus-Host Disease (GVHD)
Authors: Aliana Meneses Ferreira, Vinicius Campos Molla, Maria Cristina Nunez Seiwald, Roberta Shcolnik Szor, Pedro Henrique Arruda De Moraes, Ana Rita Da Fonseca, Mariana Serpa, Erick Menezes Xavier, Luciana Tucunduva, Yana Novis, Celso Arrais-Rodrigues
Journal: Blood (2020)