tbuckley/cabot-search huggingface dataset:
CD44 Promotes PD-L1 Expression and Its Tumor-Intrinsic Function in Breast and Lung Cancers
Authors: Tim Kong, Ryuhjin Ahn, Kangning Yang, Xianbing Zhu, Zheng Fu, Geneviève Morin, Rachel Bramley, Nikki C. Cliffe, Yibo Xue, Hellen Kuasne, Qinghao Li, Sungmi Jung, Anne V. Gonzalez, Sophie Camilleri-Broet, Marie-Christine Guiot, Morag Park, Josie Ursini-Siegel, Sidong Huang
Journal: Cancer Research (2019)

Abstract The PD-L1 (CD274) immune-checkpoint ligand is often upregulated in cancers to inhibit T cells and elicit immunosuppression. Independent of this activity, PD-L1 has recently been shown to also exert a cancer cell–intrinsic function promoting tumorigenesis. Here, we establish this tumor-intrinsic role of PD-L1 in triple-negative breast cancer (TNBC) and non–small cell lung cancer (NSCLC). Using FACS-assisted shRNA screens, we identified the cell-surface adhesion receptor CD44 as a key positive regulator of PD-L1 expression in these cancers. Mechanistically, CD44 activated PD-L1 transcription in part through its cleaved intracytoplasmic domain (ICD), which bound to a regulatory region of the PD-L1 locus containing a consensus CD44-ICD binding site. Supporting this genetic interaction, CD44 positively correlated with PD-L1 expression at the mRNA and protein levels in primary tumor samples of TNBC and NSCLC patients. These data provide a novel basis for CD44 as a critical therapeutic target to suppress PD-L1 tumor–intrinsic function. Significance: CD44 is a potential target to suppress PD-L1 function in TNBC. This finding has the potential to open a new area of therapy for TNBC.
Anti-Rh Serum Nomenclature
Authors: H. S. Baar
Journal: BMJ (1948)

The commonly used sera are anti-RhC, anti-RhD, anti-RhE, and anti-Rhc.Thus Rh+CDE would mean a blood reacting with all the four above-mentioned sera; Rh+ CDEC would mean a blood reacting with the three first-named sera but failing to react with anti-Rhc; while Rh+CDE would mean that only three sera were used for the tests.The genes could be designated as c c RD, RD, etc. Reporting " genotypes " it should be always e e stated whether the definite genotype was found out by family investigations or the most probable assumed because of its frequency.A serological " genotyping" ig only a theoretical possibility because six different sera would be nece$sary for this purpose, and even more if the five allelomorphs of C and the three of D are taken into account.The term Rh-negative should be used for the genotype rr only, which is a brief ex- c c pression for RdRd-the latter designation being thus une e necessary and can be ascertained by serological examination of the single blood sample alone.The use of the designation Rh-negative for all individuals failing to react with the anti- RhD serum involves in practice a danger.Thus individuals of c c the genotype RdRd may form anti-RhD agglutinins and are e eto be considered as Rh-negative when recipients or prospective mothers, but they may also initiate the formation of anti-RhC agglutinins and must be considered as Rh-positive when used as donors in blood transfusion.-Iam, etc., Birmingham.
Aerobic Exercise Induces Cardiac Fat Loss and Alters Cardiac Muscle Mass Through an Interleukin-6 Receptor–Dependent Mechanism
Authors: Regitse Højgaard Christensen, Louise Lang Lehrskov, Anne-Sophie Wedell-Neergaard, Grit Elster Legaard, Mathias Ried-Larsen, Kristian Karstoft, Rikke Krogh-Madsen, Bente Klarlund Pedersen, Helga Ellingsgaard, Jaya Birgitte Rosenmeier
Journal: Circulation (2019)
Natural History of Skeletal Related Events in Patients with Multiple Myeloma Who Received First- and Second- Line Therapy with Novel Agents: Results from a Single Center Analysis in 620 Patients
Authors: Evangelos Terpos, Nikolaos Kanellias, Eftathios Kastritis, Maria Gavriatopoulou, Vassilis Koutoulidis, Ioannis Ntanasis-Stathopoulos, Aristea-Maria Papanota, Despina Fotiou, Magdalini Migkou, Evangelos Eleutherakis-Papaiakovou, Panagiotis Malandrakis, Tina Bagratuni, Maria Roussou, Lia A. Moulopoulos, Meletios A. Dimopoulos
Journal: Blood (2019)
DDIS-30. EVALUATION OF THE SUSCEPTIBILITY OF NEURONS DERIVED FROM HUMAN INDUCED PLURIPOTENT STEM CELLS TO ANTICANCER DRUGS FOR CNS TUMORS
Authors: Yonehiro Kanemura, Hayato Fukusumi, Yukako Handa, Tomoko Shofuda
Journal: Neuro-Oncology (2019)

Abstract Various chemical substances, including pharmaceuticals, pose potential risks of inducing acute or delayed neurotoxicity in adults and causing developmental neurotoxicity in fetuses or children. To ensure the safety of chemical substances and drugs, neurotoxicity risk assessment is critical, and an appropriate evaluation platform for neurotoxicity is desired. At present, several anticancer reagents, including temozolomide, cisplatin, and etoposide, are used for treatment of high-grade astrocytic tumors or medulloblastomas. In comparison to lots of information about anti-tumor cells effects of these reagents, their neurotoxicity to normal neurons, especially human derived cells, have been poorly investigated because of the low accessibility of human central nervous system (CNS) tissues, the technical difficulties related to neuron isolation from adult human CNS tissues, and the higher ethical controversy surrounding the use of human CNS tissues and/or fetal cells compared to animal tissues or cells. In this study, to overcome these issues, we made human induced pluripotent stem cells derived neurons (hiPSC-neurons) for preparing alternative assay for in vitro test using primary human neuronal cells, and evaluated their susceptibility to six commonly used anticancer drugs (temozolomide, nimustine, cisplatin, etoposide, mercaptopurine, and methotrexate). Human iPSC-neurons were differentiated using 5-week monolayer culture from hiPSC-derived neural stem/progenitor cells (hiPSC-NSPCs) established by combination the dual SMAD inhibition method with neurosphere culture. In vitro cytotoxic effects of six drugs on hiPSC-neurons and their parental hiPSC-NSPCs were evaluated by ATP assay and immunocytostaining. The hiPSC-neurons were generally more resistant to the anticancer drugs than hiPSC-NSPCs, although a high dose of cisplatin decreased the levels of the neuronal marker protein ELAVL3/4 in the hiPSC-neurons after a 48-h drug treatment. These results suggest that our methodology is potentially applicable for efficient determination of the toxicity of any drug to hiPSC-neurons.
An Educational Study Promoting the Delivery of TCD Screening in Paediatric Sickle Cell Disease: A European Multi-Centre Perspective
Authors: Baba PD Inusa, Corrina Macmahon, Laura Sainati, Raffaella Colombatti, Maddalena Casale, Patrizia Rampazzo, Silverio Perrotta, Soundrie Padayachee
Journal: Blood (2019)
Prevention of Dementia—Thinking Beyond the Age and Amyloid Boxes
Authors: Sudha Seshadri
Journal: JAMA Neurology (2019)

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 Neurology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Neurology journal
Long-Term Durability of Eltrombopag Clinical Benefit for Advanced Myelodysplastic Syndromes or Acute Myeloid Leukemia and Severe Thrombocytopenia (ASPIRE Part 3)
Authors: Moshe Mittelman, Uwe Platzbecker, Boris Afanasyev, Sebastian Grosicki, Maria Socorro O Portella, Zewen Zhu, Dominik Selleslag
Journal: Blood (2019)
Severe Contralateral Striatal Hypometabolism in a Case of Diabetic Nonketotic Hyperglycemic Hemichorea on 18F-FDG PET/CT Brain
Authors: Shelvin Kumar Vadi, Sahil Mehta, Rajender Kumar, Naresh Tandyala, Harmandeep Singh, Bhagwant Rai Mittal
Journal: Clinical Nuclear Medicine (2019)

Chorea induced by diabetic nonketotic hyperglycemia is a rare and poorly understood entity with a favorable prognosis after correction of the hyperglycemia. We present a case of elderly diabetic woman with poorly controlled blood glucose levels, presenting with choreiform movements limited to the right side. F-FDG PET/CT showed marked hypometabolism in the basal ganglia contralateral to the side with hemichorea. The metabolic dysfunctions lead to nonketotic hyperglycemic chorea, although poorly understood; the index case demonstrated severe glucose hypometabolism in the striatum and adds to the other reported differential diagnoses for striatal hypometabolism.
Integrin-Mediated Adhesion to Extracellular Matrix Protein Fibronectin Drives Megakaryocytosis in JAK2V617F+ Primary Myelofibrosis
Authors: Shinobu Matsuura, Cristal Reyna Thompson, Seng Kah Ng, Aikaterini Karagianni, Christina Ward Torres, Carla Silvana Mazzeo, Orly Leiva, Alessandro Malara, Alessandra Balduini, Katya Ravid
Journal: Blood (2019)
TP53 State Dictates Genome Stability, Clinical Presentation and Outcomes in Myelodysplastic Syndromes
Authors: Elsa Bernard, Yasuhito Nannya, Tetsuichi Yoshizato, Robert P. Hasserjian, Ryunosuke Saiki, Yusuke Shiozawa, Sean M. Devlin, Heinz Tuechler, Araxe Sarian, Luca Malcovati, Francesc Sole, Detlef Haase, Maria Creignou, Max Levine, Ulrich Germing, Catherine Cargo, Yanming Zhang, Juan Medina, Juan E. Arango Ossa, Julie Schanz, Arjan van de Loosdrecht, Martin Jädersten, John M. Bennett, Magnus Tobiasson, Olivier Kosmider, Matilde Y Follo, Felicitas Thol, Ronald F Pinheiro, Valeria Santini, Ioannis Kotsianidis, Jacqueline Boultwood, Fabio PS Santos, Senji Kasahara, Takayuki Ishikawa, Hisashi Tsurumi, Akifumi Takaori-Kondo, Toru Kiguchi, Chantana Polprasert, Virginia M. Klimek, Michael R. Savona, Monika Belickova, Christina Ganster, Lionel Ades, Matteo Giovanni Della Porta, Alexandra Smith, Yesenia Werner, Minal A Patel, Agnes Viale, Katelynd Vanness, Donna S Neuberg, Kristen E. Stevenson, Kamal Menghrajani, Kelly Bolton, Pierre Fenaux, Andrea Pellagatti, Uwe Platzbecker, Michael Heuser, Peter Valent, Shigeru Chiba, Yasushi Miyazaki, Carlo Finelli, Maria Teresa Voso, Lee-Yung Shih, Michaela Fontenay, Joop H. Jansen, José Cervera, Yoshiko Atsuta, Norbert Gattermann, Benjamin L. Ebert, Rafael Bejar, Peter L Greenberg, Mario Cazzola, Eva Hellstrom Lindberg, Seishi Ogawa, Elli Papaemmanuil
Journal: Blood (2019)
Safety and Efficacy of Mitoxantrone Hydrochloride Liposome in Patients with Relapsed or Refractory Peripheral T-Cell Lymphoma and Extranodal NK/T-Cell Lymphoma: A Multicenter, Single-Arm, Open-Label, Phase 2 Clinical Trial
Authors: Hui-qiang Huang, Yunhong Huang, Gao Yan, Haiyan Yang, Qingyuan Zhang, Runxiang Yang, Min Zhou, Yufu Li, Yan Li, Lihong Liu, Hui Zhou, Hongmei Jing, Zhigang Peng, Ding Yu, Rong yan Zhang, Bing Xu, Xiaohong Zhang, Junyuan Qi, Liping MA, Shan Chen, Jianfei Xue
Journal: Blood (2019)
A Critical Role for Neocortical Processing of Threat Memory
Authors: Tamas Dalmay, Elisabeth Abs, Rogier B. Poorthuis, Jan Hartung, De-Lin Pu, Sebastian Onasch, Yave R. Lozano, Jérémy Signoret-Genest, Philip Tovote, Julijana Gjorgjieva, Johannes J. Letzkus
Journal: Neuron (2019)
The clinical value of detecting microcalcifications on a mammogram
Authors: Tibor Tot, Maria Gere, Syster Hofmeyer, Annette Bauer, Ulrika Pellas
Journal: Seminars in Cancer Biology (2019)

Many breast lesions are associated with microcalcifications that are detectable by mammography. In most cases, radiologists are able to distinguish calcifications usually associated with benign diseases from those associated with malignancy. In addition to their value in the early detection of breast carcinoma and accurate radiological diagnosis, the presence of microcalcifications often affects the extent of surgical intervention. Certain types of microcalcifications are associated with negative genetic and molecular characteristics of the tumor and unfavorable prognosis. Microcalcifications localized in the larger ducts (duct-centric, casting-type microcalcifications) represent an independent negative prognostic marker compared to lesions containing other types of microcalcifications and to non-calcified lesions. In this review, we summarize the theoretical and methodological background for understanding the clinical impact and discuss the diagnostic and prognostic value of microcalcifications detected in the breast by mammography.
Cytotoxic T-Cell Responses (CTL) Against Several Leukemia-Associated-Antigens (LAA) Related to the Detected Cytokine Profile in the Course of Allogeneic Hematopoietic Stem Cell Transplantation (allo-HSCT) and Donor Lymphocyte Infusion (DLI) in Patients with Different Hematological Diseases
Authors: Susanne Hofmann, Marlies Götz, Cornelia Herbst, Vanessa Schneider, Markus Wiesneth, Donald Bunjes, Hartmut Döhner, Jochen Greiner
Journal: Blood (2014)
Polyfunctional, Proinflammatory, Tissue‐Resident Memory Phenotype and Function of Synovial Interleukin‐17A+<scp>CD</scp>8+ T Cells in Psoriatic Arthritis
Authors: Kathryn J. A. Steel, Ushani Srenathan, Michael Ridley, Lucy E. Durham, Shih‐Ying Wu, Sarah E. Ryan, Catherine D. Hughes, Estee Chan, Bruce W. Kirkham, Leonie S. Taams
Journal: Arthritis & Rheumatology (2019)

Objective Genetic associations imply a role for CD 8+ T cells and the interleukin‐23 ( IL ‐23)/ IL ‐17 axis in psoriatic arthritis (PsA) and other spondyloarthritides (SpA). IL ‐17A+ CD 8+ (Tc17) T cells are enriched in the synovial fluid ( SF ) of patients with PsA, and IL ‐17A blockade is clinically efficacious in PsA/SpA. This study was undertaken to determine the immunophenotype, molecular profile, and function of synovial Tc17 cells in order to elucidate their role in PsA/SpA pathogenesis. Methods Peripheral blood ( PB ) and SF mononuclear cells were isolated from patients with PsA or other types of SpA. Cells were phenotypically, transcriptionally, and functionally analyzed by flow cytometry (n = 6–18), T cell receptor β ( TCR β) sequencing (n = 3), RNA ‐Seq (n = 3), quantitative reverse transcriptase–polymerase chain reaction (n = 4), and Luminex or enzyme‐linked immunosorbent assay (n = 4–16). Results IL ‐17A+ CD 8+ T cells were predominantly TCR αβ+ and their frequencies were increased in the SF versus the PB of patients with established PsA ( P &lt; 0.0001) or other SpA ( P = 0.0009). TCR β sequencing showed that these cells were polyclonal in PsA (median clonality 0.08), while RNA ‐Seq and deep immunophenotyping revealed that PsA synovial Tc17 cells had hallmarks of Th17 cells ( RORC / IL 23R/ CCR 6 / CD 161 ) and Tc1 cells (granzyme A/B). Synovial Tc17 cells showed a strong tissue‐resident memory T (Trm) cell signature and secreted a range of proinflammatory cytokines. We identified CXCR 6 as a marker for synovial Tc17 cells, and increased levels of CXCR 6 ligand CXCL 16 in PsA SF ( P = 0.0005), which may contribute to their retention in the joint. Conclusion Our results identify synovial Tc17 cells as a polyclonal subset of Trm cells characterized by polyfunctional, proinflammatory mediator production and CXCR 6 expression. The molecular signature and functional profiling of these cells may help explain how Tc17 cells can contribute to synovial inflammation and disease persistence in PsA and possibly other types of SpA.
GENE-23. GENOME-WIDE DNA METHYLATION PROFILES DISTINGUISH SILENT FROM NON-SILENT ACTH ADENOMAS
Authors: Franz Ricklefs, Krys Fita, Roman Rotermund, Manfred Westphal, Ulrich Schüller, Joerg Flitsch
Journal: Neuro-Oncology (2019)

Abstract BACKGROUND Corticotroph adenomas are immunopositive for adrenocorticotrophic hormone (ACTH) associated with elevated blood ACTH levels leading to Cushing disease (CD). Yet silent ACTH adenomas (SCA) immunostain for ACTH but do not cause hypercortisolism. SCA have consistently been shown to have a more aggressive postoperative course, then nonfunctioning and ACTH adenomas. Here we show that genome-wide methylation profiles can be used to distinguish ACTH adenomas from SCA. METHODS16 SCA patients and 19 CD patients that underwent transsphenoidal resection were included. Tumor size was measured by MRI. Tumor histology was proven by immunstain for ACTH and routine histopathology. Sanger sequencing was performed to analyse mutational burden within the ACTH locus (n=3). Genome-wide DNA methylation profiling was performed using a 850k Illumina EPIC array and classified by the DKFZ brain tumor classifier as well as PCA analysis using R (n=17). RESULTS Mean age was 55,4 and 46,2 for SCA and CD patients, respectively. Patients with SCA had significantly larger tumors (SCA: 12,56±3,07ccm; CD: 1,9±1,2ccm p&lt; 0.01). Both SCA and CD tumors showed strong expression of ACTH as proven by immunohistochemistry. Sanger sequencing revealed no mutations within the ACTH gene locus in SCA. Both, SCA and CD tumors classified as ACTH adenomas by genome-wide methylation profiling. Further PCA of DNA methylation profiles allowed subtype tumor classification into SCA and CD adenomas. CONCLUSION SCA show a strong expression of ACTH without causing hypercortisolism. The reason for this is not yet known. Our data suggest that SCA do not harbor specific mutations within the ACTH gene locus. However genome wide methylation profiles allows subgrouping of SCA and CD adenomas.
Reduction of Vertebral Bone Density in Patients with Hodgkin Lymphoma Above 30 Years of Age Correlates with the Cumulative Dose of Steroids They Receive As Part of Treatment Protocol
Authors: Nadav Ofshenko, Eyal Bercovich, Tania Mashiach, Michal Weiler-Sagie, Daniela Militianu, Eldad J Dann
Journal: Blood (2019)
Abstract 11985: Device-Based Phrenic Nerve Stimulation for Central Sleep Apnea: Interventional Approaches Increase Implantation Success - Single Center Experience
Authors: Klaus J Gutleben, Henrik Fox, Thomas Fischbach, Britta Körber, Vanessa Rubesch-Kütemeyer, Denise Guckel, Dieter Horstkotte, Georg Nölker
Journal: Circulation (2018)

Introduction: Device based phrenic nerve stimulation (PNS) for central sleep apnea (CSA) has been shown to be effective and safe. Transvenous PNS lead implantation can be difficult due to anatomica...
TMIC-04. CANCER STEM CELL GENETIC AND GENOMIC ALTERATIONS DIFFERENTIALLY DICTATE STROMAL CELL REGULATION OF LOW-GRADE GLIOMA GROWTH
Authors: Xiaofan Guo, Yuan Pan, David Gutmann
Journal: Neuro-Oncology (2019)

Abstract BACKGROUND Children with the Neurofibromatosis type 1 (NF1) brain tumor predisposition syndrome are prone to the formation of low-grade gliomas (LGGs) of the optic pathway (optic pathway glioma; OPG). While all tumors harbor bi-allelic NF1 gene inactivation, there is significant clinical variability in affected children with respect to tumor growth, associated neurologic deficits, and response to therapy. In order to identify the potential factors that contribute to glioma biological variability, we leveraged a series of Nf1 mutant optic glioma mouse strains with different germline Nf1 gene mutations and secondary genomic alterations. METHODS Cancer stem cells (optic glioma stem cells; o-GSCs) were isolated from these Nf1 mutant optic glioma mouse strains, and their intrinsic growth properties and chemokine expression profiles determined. RESULTS Differences in the intrinsic o-GSC growth properties did not account for the observed differences in Nf1 optic glioma tumor growth. Instead, Nf1 optic glioma tumor growth correlated with the differential recruitment of T cells and microglia by chemokines produced by the o-GSCs. As such, the collective action of T cells and microglia dictated the level of Ccl5 expression, the key stromal factor that determines murine NF1-associated optic glioma growth. CONCLUSIONS Taken together, these observations demonstrate that genomic and genetic differences within the cancer cells create unique Nf1 optic glioma growth patterns through the differential elaboration of chemokines that attract T cells and microglia. GRANT SUPPORT: This work was funded by grants from the National Cancer Institute (1-R01-CA195692-01) and the National Institute of Neurological Disorders and Stroke (1-R35-NS07211-01) to D.H.G, as well as to the Hope Center Viral Vectors Core and the Genome Technology Access Center (UL1-TR000448). Y.P. was supported by a fellowship grant from the James S. McDonnell Foundation.
INNV-30. RESPONSE WITH COMBINED DABRAFENIB AND TRAMETINIB AFTER BRAF INHIBITOR FAILURE IN BRAF-MUTATED GLIOBLASTOMA: A CASE REPORT
Authors: Marina Kushnirsky, Macarena I De la Fuente, Lynn Feun
Journal: Neuro-Oncology (2019)

Abstract Glioblastoma (GBM) carries a poor prognosis despite aggressive multimodality therapy. Oncogenic BRAF mutations are present in &lt; 2% of GBM, along with other glioma types (ganglioglioma, pleomorphic xanthoastrocytoma). Although oral inhibitors of the oncogenic BRAFv600 kinase have demonstrated some efficacy in GBM, several mechanisms mediating resistance to BRAF inhibitors through MAPK reactivation have been described. BRAF inhibitor monotherapy is also associated with an increased risk for hyperproliferative skin lesions. We present a case of a 44-year-old man who initially presented with headaches and seizures and was diagnosed with a left temporal, MGMT unmethylated, BRAF V600E mutant GBM. He underwent gross total resection followed by radiation therapy with concurrent temozolomide, followed by 9 cycles of adjuvant temozolomide. He presented with progression of disease (POD) and subsequently failed treatment with carboplatin after two cycles (first recurrence). He had a repeat resection, and was enrolled in a clinical trial of autologous dendritic cell vaccine and presented with POD after 10 months on this treatment (second recurrence). He was started on another clinical trial of BRAF inhibitor, achieving partial response but developed POD after 7 months on this therapy (third recurrence). He was started on BRAF inhibitor dabrafenib and MEK inhibitor trametinib (D+T), achieving complete response. At the time of this report, 8 months after initiating treatment, the patient remains clinically stable with MRI showing CR. To our knowledge, this is the first report of clinical and radiographic response to combined D+T after BRAF inhibitor failure in BRAF-mutated glioblastoma. Several ongoing trials (NCT01677741, NCT01748149, NCT02124772, NCT02684058, NCT02285439), will elucidate the precise role of these drugs as single agent and in combination in pediatric and adult brain tumors.
BACTERIAL ENDOCARDITIS AND UROLOGY.
Authors: J. D. LLOYD-STILL
Journal: BMJ (1965)

Although bacterial endocarditis in relation to surgery and manipulation of the lower urinary tract has been stressed in the American literature, there have been comparatively few reports in the British journals, though some of the earlier observations on bacteraemia following urethral manipulations were reported in this country. Three cases of bacterial endocarditis were seen by me in these hospitals recently. On analysing the post-mortem reports since 1955, three further cases were proved at necropsy.
Molecular Characteristics That Predict Response to Azacitidine Therapy
Authors: Yasuhito Nannya, Magnus Tobiasson, Elsa Bernard, Shinya Sato, Maria Creignou, June Takeda, Lanying Zhao, Yuichi Shiraishi, Kenichi Chiba, Hiroko Tanaka, Hisashi Tsurumi, Senji Kasahara, Masataka Taguchi, Akifumi Kondo Takaori, Kazuma Ohyashiki, Hideki Makishima, Kenichi Yoshida, Tomoki Naoe, Yasushi Miyazaki, Satoru Miyano, Elli Papaemmanuil, Eva Hellstrom Lindberg, Seishi Ogawa
Journal: Blood (2019)