Journal Cover Blood
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   ISSN (Print) 0006-4971 - ISSN (Online) 1528-0020
   Published by American Society of Hematology Homepage  [1 journal]
  • Distinct miRNA profile in prognosis of early CTCL
    • Authors: Wasik M. A.
      Pages: 711 - 711
      Keywords: Free Research Articles
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2017-12-821520
      Issue No: Vol. 131, No. 7 (2018)
       
  • BRD4: epigenetic origin and target of CTCL
    • Authors: Zhao, X; Tao, J.
      Pages: 712 - 713
      Keywords: Free Research Articles
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2017-12-820266
      Issue No: Vol. 131, No. 7 (2018)
       
  • Only the strong: when antibodies hold on
    • Authors: Thomas W. E.
      Pages: 713 - 714
      Keywords: Free Research Articles
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2017-12-821561
      Issue No: Vol. 131, No. 7 (2018)
       
  • Clot structure predicts recurrent thrombosis
    • Authors: White N. J.
      Pages: 715 - 716
      Keywords: Free Research Articles
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2018-01-824169
      Issue No: Vol. 131, No. 7 (2018)
       
  • A landscape of germ line mutations in a cohort of inherited bone marrow
           failure patients
    • Authors: Bluteau, O; Sebert, M, Leblanc, T, Peffault de Latour, R, Quentin, S, Lainey, E, Hernandez, L, Dalle, J.-H, Sicre de Fontbrune, F, Lengline, E, Itzykson, R, Clappier, E, Boissel, N, Vasquez, N, Da Costa, M, Masliah-Planchon, J, Cuccuini, W, Raimbault, A, De Jaegere, L, Ades, L, Fenaux, P, Maury, S, Schmitt, C, Muller, M, Domenech, C, Blin, N, Bruno, B, Pellier, I, Hunault, M, Blanche, S, Petit, A, Leverger, G, Michel, G, Bertrand, Y, Baruchel, A, Socie, G, Soulier, J.
      Pages: 717 - 732
      Abstract: Bone marrow (BM) failure (BMF) in children and young adults is often suspected to be inherited, but in many cases diagnosis remains uncertain. We studied a cohort of 179 patients (from 173 families) with BMF of suspected inherited origin but unresolved diagnosis after medical evaluation and Fanconi anemia exclusion. All patients had cytopenias, and 12.0% presented ≥5% BM blast cells. Median age at genetic evaluation was 11 years; 20.7% of patients were aged ≤2 years and 36.9% were ≥18 years. We analyzed genomic DNA from skin fibroblasts using whole-exome sequencing, and were able to assign a causal or likely causal germ line mutation in 86 patients (48.0%), involving a total of 28 genes. These included genes in familial hematopoietic disorders (GATA2, RUNX1), telomeropathies (TERC, TERT, RTEL1), ribosome disorders (SBDS, DNAJC21, RPL5), and DNA repair deficiency (LIG4). Many patients had an atypical presentation, and the mutated gene was often not clinically suspected. We also found mutations in genes seldom reported in inherited BMF (IBMF), such as SAMD9 and SAMD9L (N = 16 of the 86 patients, 18.6%), MECOM/EVI1 (N = 6, 7.0%), and ERCC6L2 (N = 7, 8.1%), each of which was associated with a distinct natural history; SAMD9 and SAMD9L patients often experienced transient aplasia and monosomy 7, whereas MECOM patients presented early-onset severe aplastic anemia, and ERCC6L2 patients, mild pancytopenia with myelodysplasia. This study broadens the molecular and clinical portrait of IBMF syndromes and sheds light on newly recognized disease entities. Using a high-throughput sequencing screen to implement precision medicine at diagnosis can improve patient management and family counseling.
      Keywords: Hematopoiesis and Stem Cells, Pediatric Hematology, Plenary Papers, Free Research Articles, Myeloid Neoplasia, Red Cells, Iron, and Erythropoiesis, CME article, Clinical Trials and Observations
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2017-09-806489
      Issue No: Vol. 131, No. 7 (2018)
       
  • How I use catheter-directed interventional therapy to treat patients with
           venous thromboembolism
    • Authors: Vedantham, S; Sista, A. K.
      Pages: 733 - 740
      Abstract: Patients who present with severe manifestations of acute venous thromboembolism (VTE) are at higher risk for premature death and long-term disability. In recent years, catheter-based interventional procedures have shown strong potential to improve clinical outcomes in selected VTE patients. However, physicians continue to be routinely faced with challenging decisions that pertain to the utilization of these risky and costly treatment strategies, and there is a relative paucity of published clinical trials with sufficient rigor and directness to inform clinical practice. In this article, using 3 distinct clinical scenario presentations, we draw from the available published literature describing the natural history, pathophysiology, treatments, and outcomes of VTE to illustrate the key factors that should influence clinical decision making for patients with severe manifestations of deep vein thrombosis and pulmonary embolism. The results of a recently completed pivotal multicenter randomized trial are also discussed.
      Keywords: How I Treat, Free Research Articles, Thrombosis and Hemostasis
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2016-11-693663
      Issue No: Vol. 131, No. 7 (2018)
       
  • Copper 64-labeled daratumumab as a PET/CT imaging tracer for multiple
           myeloma
    • Authors: Caserta, E; Chea, J, Minnix, M, Viola, D, Vonderfecht, S, Yazaki, P, Crow, D, Khalife, J, Sanchez, J. F, Palmer, J. M, Hui, S, Carlesso, N, Keats, J, Kim, Y, Buettner, R, Marcucci, G, Rosen, S, Shively, J, Colcher, D, Krishnan, A, Pichiorri, F.
      Pages: 741 - 745
      Abstract: As a growing number of patients with multiple myeloma (MM) respond to upfront therapies while eventually relapsing in a time frame that is often unpredictable, attention has increasingly focused on developing novel diagnostic criteria to also account for disease dissemination. Positron emission tomography/computed tomography (PET/CT) is often used as a noninvasive monitoring strategy to assess cancer cell dissemination, but because the uptake of the currently used radiotracer 18fluorodeoxyglucose (18F-FDG) is a function of the metabolic activity of both malignant and nonmalignant cells, the results frequently lack sufficient specificity. Radiolabeled antibodies targeting MM tissue may detect disease irrespective of cell metabolism. Hence, we conjugated the clinically significant CD38-directed human antibody daratumumab (Darzalex [Dara]) to the DOTA chelator and labeled it with the positron-emitting radionuclide copper 64 (64Cu; 64Cu-DOTA-Dara). Here, we show that 64Cu-DOTA-Dara can efficiently bind CD38 on the surface of MM cells and was mainly detected in the bones associated with tumor in a MM murine model. We also show that PET/CT based on 64Cu-DOTA-Dara displays a higher resolution and specificity to detect MM cell dissemination than does 18F-FDG PET/CT and was even more sensitive than were bioluminescence signals. We therefore have supporting evidence for using 64Cu-DOTA-Dara as a novel imaging agent for MM.
      Keywords: Immunobiology and Immunotherapy, Brief Reports
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2017-09-807263
      Issue No: Vol. 131, No. 7 (2018)
       
  • An APRIL-based chimeric antigen receptor for dual targeting of BCMA and
           TACI in multiple myeloma
    • Authors: Lee, L; Draper, B, Chaplin, N, Philip, B, Chin, M, Galas-Filipowicz, D, Onuoha, S, Thomas, S, Baldan, V, Bughda, R, Maciocia, P, Kokalaki, E, Neves, M. P, Patel, D, Rodriguez-Justo, M, Francis, J, Yong, K, Pule, M.
      Pages: 746 - 758
      Abstract: B-cell maturation antigen (BCMA) is a promising therapeutic target for multiple myeloma (MM), but expression is variable, and early reports of BCMA targeting chimeric antigen receptors (CARs) suggest antigen downregulation at relapse. Dual-antigen targeting increases targetable tumor antigens and reduces the risk of antigen-negative disease escape. "A proliferation-inducing ligand" (APRIL) is a natural high-affinity ligand for BCMA and transmembrane activator and calcium-modulator and cyclophilin ligand (TACI). We quantified surface tumor expression of BCMA and TACI on primary MM cells (n = 50). All cases tested expressed BCMA, and 39 (78%) of them also expressed TACI. We engineered a third-generation APRIL-based CAR (ACAR), which killed targets expressing either BCMA or TACI (P < .01 and P < .05, respectively, cf. control, effector-to-target [E:T] ratio 16:1). We confirmed cytolysis at antigen levels similar to those on primary MM, at low E:T ratios (56.2% ± 3.9% killing of MM.1s at 48 h, E:T ratio 1:32; P < .01) and of primary MM cells (72.9% ± 12.2% killing at 3 days, E:T ratio 1:1; P < .05, n = 5). Demonstrating tumor control in the absence of BCMA, we maintained cytolysis of primary tumor expressing both BCMA and TACI in the presence of a BCMA-targeting antibody. Furthermore, using an intramedullary myeloma model, ACAR T cells caused regression of an established tumor within 2 days. Finally, in an in vivo model of tumor escape, there was complete ACAR-mediated tumor clearance of BCMA+TACI– and BCMA–TACI+ cells, and a single-chain variable fragment CAR targeting BCMA alone resulted in outgrowth of a BCMA-negative tumor. These results support the clinical potential of this approach.
      Keywords: Multiple Myeloma, Immunobiology and Immunotherapy, Lymphoid Neoplasia
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2017-05-781351
      Issue No: Vol. 131, No. 7 (2018)
       
  • Prognostic miRNA classifier in early-stage mycosis fungoides: development
           and validation in a Danish nationwide study
    • Authors: Lindahl, L. M; Besenbacher, S, Rittig, A. H, Celis, P, Willerslev-Olsen, A, Gjerdrum, L. M. R, Krejsgaard, T, Johansen, C, Litman, T, Woetmann, A, Odum, N, Iversen, L.
      Pages: 759 - 770
      Abstract: Mycosis fungoides (MF) is the most frequent form of cutaneous T-cell lymphoma. The disease often takes an indolent course, but in approximately one-third of the patients, the disease progresses to an aggressive malignancy with a poor prognosis. At the time of diagnosis, it is impossible to predict which patients develop severe disease and are in need of aggressive treatment. Accordingly, we investigated the prognostic potential of microRNAs (miRNAs) at the time of diagnosis in MF. Using a quantitative reverse transcription polymerase chain reaction platform, we analyzed miRNA expression in diagnostic skin biopsies from 154 Danish patients with early-stage MF. The patients were subdivided into a discovery cohort (n = 82) and an independent validation cohort (n = 72). The miRNA classifier was built using a LASSO (least absolute shrinkage and selection operator) Cox regression to predict progression-free survival (PFS). We developed a 3-miRNA classifier, based on miR-106b-5p, miR-148a-3p, and miR-338-3p, which successfully separated patients into high-risk and low-risk groups of disease progression. PFS was significantly different between these groups in both the discovery cohort and the validation cohort. The classifier was stronger than existing clinical prognostic factors and remained a strong independent prognostic tool after stratification and adjustment for these factors. Importantly, patients in the high-risk group had a significantly reduced overall survival. The 3-miRNA classifier is an effective tool to predict disease progression of early-stage MF at the time of diagnosis. The classifier adds significant prognostic value to existing clinical prognostic factors and may facilitate more individualized treatment of these patients.
      Keywords: Free Research Articles, Lymphoid Neoplasia
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2017-06-788950
      Issue No: Vol. 131, No. 7 (2018)
       
  • Diminished microRNA-29b level is associated with BRD4-mediated activation
           of oncogenes in cutaneous T-cell lymphoma
    • Authors: Kohnken, R; Wen, J, Mundy-Bosse, B, McConnell, K, Keiter, A, Grinshpun, L, Hartlage, A, Yano, M, McNeil, B, Chakravarti, N, William, B, Bradner, J. E, Caligiuri, M. A, Porcu, P, Mishra, A.
      Pages: 771 - 781
      Abstract: MicroRNA (miRNA) dysregulation is a hallmark of cutaneous T-cell lymphoma (CTCL), an often-fatal malignancy of skin-homing CD4+ T cells for which there are few effective therapies. The role of microRNAs (miRs) in controlling epigenetic modifier-dependent transcriptional regulation in CTCL is unknown. In this study, we characterize a novel miR dysregulation that contributes to overexpression of the epigenetic reader bromodomain-containing protein 4 (BRD4). We used patient CD4+ T cells to show diminished levels of miR-29b compared with healthy donor cells. Patient cells and miR-29b–/– mouse cells revealed an inverse relationship between miR-29b and BRD4, the latter of which is overexpressed in these cells. Chromatin immunoprecipitation and sequencing analysis revealed increased genome-wide BRD4 occupancy at promoter and enhancer regions in CD4+ T cells from CTCL patients. The cumulative result of BRD4 binding was increased expression of tumor-associated genes such as NOTCH1 and RBPJ, as well as the interleukin-15 (IL-15) receptor complex, the latter enhancing IL-15 autocrine signaling. Furthermore, we confirm the in vivo relevance of this pathway in our IL-15 transgenic mouse model of CTCL by showing that interference with BRD4-mediated pathogenesis, either by restoring miR-29b levels via bortezomib treatment or by directly inhibiting BRD4 binding via JQ1 treatment, prevents progression of CTCL. We describe a novel oncogenic pathway featuring IL-15, miR-29b, and BRD4 in CTCL and suggest targeting of these components as a potentially effective therapy for CTCL patients.
      Keywords: Lymphoid Neoplasia
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2017-09-805663
      Issue No: Vol. 131, No. 7 (2018)
       
  • Defining the requirements for the pathogenic interaction between mutant
           calreticulin and MPL in MPN
    • Authors: Elf, S; Abdelfattah, N. S, Baral, A. J, Beeson, D, Rivera, J. F, Ko, A, Florescu, N, Birrane, G, Chen, E, Mullally, A.
      Pages: 782 - 786
      Abstract: Mutations in calreticulin (CALR) are phenotypic drivers in the pathogenesis of myeloproliferative neoplasms. Mechanistic studies have demonstrated that mutant CALR binds to the thrombopoietin receptor MPL, and that the positive electrostatic charge of the mutant CALR C terminus is required for mutant CALR-mediated activation of JAK-STAT signaling. Here we demonstrate that although binding between mutant CALR and MPL is required for mutant CALR to transform hematopoietic cells; binding alone is insufficient for cytokine independent growth. We further show that the threshold of positive charge in the mutant CALR C terminus influences both binding of mutant CALR to MPL and activation of MPL signaling. We find that mutant CALR binds to the extracellular domain of MPL and that 3 tyrosine residues within the intracellular domain of MPL are required to activate signaling. With respect to mutant CALR function, we show that its lectin-dependent function is required for binding to MPL and for cytokine independent growth, whereas its chaperone and polypeptide-binding functionalities are dispensable. Together, our findings provide additional insights into the mechanism of the pathogenic mutant CALR-MPL interaction in myeloproliferative neoplasms.
      Keywords: Myeloid Neoplasia, Brief Reports
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2017-08-800896
      Issue No: Vol. 131, No. 7 (2018)
       
  • Fc-independent immune thrombocytopenia via mechanomolecular signaling in
           platelets
    • Authors: Quach, M. E; Dragovich, M. A, Chen, W, Syed, A. K, Cao, W, Liang, X, Deng, W, De Meyer, S. F, Zhu, G, Peng, J, Ni, H, Bennett, C. M, Hou, M, Ware, J, Deckmyn, H, Zhang, X. F, Li, R.
      Pages: 787 - 796
      Abstract: Immune thrombocytopenia (ITP) is a prevalent autoimmune disease characterized by autoantibody-induced platelet clearance. Some ITP patients are refractory to standard immunosuppressive treatments such as intravenous immunoglobulin (IVIg). These patients often have autoantibodies that target the ligand-binding domain (LBD) of glycoprotein Ibα (GPIbα), a major subunit of the platelet mechanoreceptor complex GPIb-IX. However, the molecular mechanism of this Fc-independent platelet clearance is not clear. Here, we report that many anti-LBD monoclonal antibodies such as 6B4, but not AK2, activated GPIb-IX in a shear-dependent manner and induced IVIg-resistant platelet clearance in mice. Single-molecule optical tweezer measurements of antibodies pulling on full-length GPIb-IX demonstrated that the unbinding force needed to dissociate 6B4 from the LBD far exceeds the force required to unfold the juxtamembrane mechanosensory domain (MSD) in GPIbα, unlike the AK2-LBD unbinding force. Binding of 6B4, not AK2, induced shear-dependent unfolding of the MSD on the platelet, as evidenced by increased exposure of a linear sequence therein. Imaging flow cytometry and aggregometry measurements of platelets and LBD-coated platelet-mimetic beads revealed that 6B4 can sustain crosslinking of platelets under shear, whereas 6B4 Fab and AK2 cannot. These results suggest a novel mechanism by which anti-LBD antibodies can exert a pulling force on GPIb-IX via platelet crosslinking, activating GPIb-IX by unfolding its MSD and inducing Fc-independent platelet clearance.
      Keywords: Thrombocytopenia, Platelets and Thrombopoiesis
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2017-05-784975
      Issue No: Vol. 131, No. 7 (2018)
       
  • Altered plasma clot properties increase the risk of recurrent deep vein
           thrombosis: a cohort study
    • Authors: Cieslik, J; Mrozinska, S, Broniatowska, E, Undas, A.
      Pages: 797 - 807
      Abstract: It has been demonstrated that fibrin clots generated from plasma samples obtained from patients with prior thromboembolic events are denser and less susceptible to lysis. Such a prothrombotic fibrin clot phenotype has been suggested as a new risk factor for venous thromboembolism, but its prognostic value is unclear. To assess whether abnormal clot properties can predict recurrent deep vein thrombosis (DVT), we studied 320 consecutive patients aged 18 to 70 years following the first-ever DVT. Plasma clot properties were evaluated after 3 months of anticoagulant treatment since the index event. A mean duration of anticoagulation was 10 months (range, 4-20). Recurrent DVT was observed in 77 patients (25%; 6.6%/year) during a median follow-up of 44 months. Recurrences of DVT were associated with faster formation (–9% lag phase) of denser fibrin networks (–12% fibrin clot permeability [Ks]) and 4% higher maximum absorbance of plasma clots that displayed impaired fibrinolytic degradation (+25% prolonged clot lysis time [CLT]) and a 5% slower rate of increase in D-dimer levels during clot degradation (D-Drate; all P < .05). Proximal DVT alone, higher C-reactive protein, D-dimer, peak thrombin, lower Ks, shorter lag phase, decreased D-Drate, and prolonged CLT were independent predictors of recurrences (all P < .05). Individuals characterized by low Ks (≤7.3 x 10–9 cm2) and prolonged CLT (>96 min) were at the highest risk of recurrent DVT (odds ratio, 15.8; 95% confidence interval, 7.5-33.5). Kaplan-Meier curves showed that reduced Ks and prolonged CLT predicted recurrent DVT. We demonstrate that unfavorably altered clot properties may predict recurrent DVT after anticoagulation withdrawal.
      Keywords: Thrombosis and Hemostasis
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2017-07-798306
      Issue No: Vol. 131, No. 7 (2018)
       
  • Evolutionary basis of HLA-DPB1 alleles affects acute GVHD in unrelated
           donor stem cell transplantation
    • Authors: Morishima, S; Shiina, T, Suzuki, S, Ogawa, S, Sato-Otsubo, A, Kashiwase, K, Azuma, F, Yabe, T, Satake, M, Kato, S, Kodera, Y, Sasazuki, T, Morishima, Y, for the Japan Marrow Donor Program
      Pages: 808 - 817
      Abstract: HLA-DPB1 T-cell epitope (TCE) mismatching algorithm and rs9277534 SNP at the 3' untranslated region (3'UTR) in the HLA-DPB1 gene are key factors for transplant-related events in unrelated hematopoietic cell transplantation (UR-HCT). However, the association of these 2 mechanisms has not been elucidated. We analyzed 19 frequent HLA-DPB1 alleles derived from Japanese healthy subjects by next-generation sequencing of the entire HLA-DPB1 gene region and multi-SNP data of the HLA region in 1589 UR-HCT pairs. The risk of acute graft-versus-host disease (aGVHD) was analyzed in 1286 patients with single HLA-DPB1 mismatch UR-HCT. The phylogenetic tree constructed using the entire gene region demonstrated that HLA-DPB1 alleles were divided into 2 groups, HLA-DP2 and HLA-DP5. Although a phylogenetic relationship in the genomic region from exon 3 to 3'UTR (Ex3-3'UTR) obviously supported the division of HLA-DP2 and HLA-DP5 groups, which in exon 2 showed intermingling of HLA-DPB1 alleles in a non–HLA-DP2 and non–HLA-DP5-group manner. Multi-SNP data also showed 2 discriminative HLA-DPB1 groups according to Ex3-3'UTR. Risk of grade 2-4 aGVHD was significantly higher in patient HLA-DP5 group mismatch than patient HLA-DP2 group mismatch (hazard ratio, 1.28; P = .005), regardless of donor mismatch HLA-DP group. Regarding TCE mismatch, increasing risk of aGVHD in patient HLA-DP5 group mismatch and TCE-nonpermissive mismatch were observed only in patients with TCE-permissive mismatch and patient HLA-DP2 group mismatch, respectively. Evolutionary analysis revealed that rs9277534 represented a highly conserved HLA-DPB1 Ex3-3'UTR region and may provoke aGVHD differently to TCE mismatching algorithm, reflecting exon 2 polymorphisms. These findings enrich our understanding of the mechanism of aGVHD in HLA-DPB1 mismatch UR-HCT.
      Keywords: Transplantation
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2017-08-801449
      Issue No: Vol. 131, No. 7 (2018)
       
  • Long-term survival of older patients with MDS treated with HMA therapy
           without subsequent stem cell transplantation
    • Authors: Zeidan, A. M; Stahl, M, Hu, X, Wang, R, Huntington, S. F, Podoltsev, N. A, Gore, S. D, Ma, X, Davidoff, A. J.
      Pages: 818 - 821
      Keywords: Myeloid Neoplasia, Clinical Trials and Observations
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2017-10-811729
      Issue No: Vol. 131, No. 7 (2018)
       
  • Five percent of healthy newborns have an ETV6-RUNX1 fusion as revealed by
           DNA-based GIPFEL screening
    • Authors: Schäfer, D; Olsen, M, Lähnemann, D, Stanulla, M, Slany, R, Schmiegelow, K, Borkhardt, A, Fischer, U.
      Pages: 821 - 826
      Keywords: Pediatric Hematology, Lymphoid Neoplasia
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2017-09-808402
      Issue No: Vol. 131, No. 7 (2018)
       
  • Loss of RKIP is a frequent event in myeloid sarcoma and promotes leukemic
           tissue infiltration
    • Authors: Caraffini, V; Perfler, B, Berg, J. L, Uhl, B, Schauer, S, Kashofer, K, Ghaffari-Tabrizi-Wizsy, N, Strobl, H, Wölfler, A, Hoefler, G, Sill, H, Zebisch, A.
      Pages: 826 - 830
      Keywords: Myeloid Neoplasia
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2017-09-804906
      Issue No: Vol. 131, No. 7 (2018)
       
  • ABO zygosity, but not secretor or Fc receptor status, is a significant
           risk factor for IVIG-associated hemolysis
    • Authors: Branch, D. R; Hellberg, A, Bruggeman, C. W, Storry, J. R, Sakac, D, Blacquiere, M, Tong, T. N, Burke-Murphy, E, Binnington, B, Parmar, N, Riden, L. S, Willie, K, Armali, C, Aziz, J, Lieberman, L, Laroche, V, Callum, J, Lin, Y, Shehata, N, Pavenski, K, Lau, W, Hannach, B, Kuijpers, T. W, Olsson, M. L, Cserti-Gazdewich, C, Pendergrast, J.
      Pages: 830 - 835
      Keywords: Transfusion Medicine
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2017-07-796151
      Issue No: Vol. 131, No. 7 (2018)
       
  • When it rains, it pours
    • Authors: Degaud, M; Sujobert, P.
      Pages: 836 - 836
      Keywords: Free Research Articles, BloodWork, Lymphoid Neoplasia
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2017-10-814087
      Issue No: Vol. 131, No. 7 (2018)
       
  • Jordans anomaly
    • Authors: Winokur, D; LiPera, W.
      Pages: 837 - 837
      Keywords: Free Research Articles, BloodWork, Phagocytes, Granulocytes, and Myelopoiesis
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2017-10-812677
      Issue No: Vol. 131, No. 7 (2018)
       
  • Genetic landscape of inherited BMF
    • Pages: 838 - 838
      Keywords: Free Research Articles, CME article
      PubDate: 2018-02-15T09:00:35-08:00
      DOI: 10.1182/blood-2017-12-823732
      Issue No: Vol. 131, No. 7 (2018)
       
 
 
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