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Journal Cover Blood
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   ISSN (Print) 0006-4971 - ISSN (Online) 1528-0020
   Published by American Society of Hematology Homepage  [1 journal]
  • Racial/ethnic disparities: need more work!
    • Authors: Landgren; O.
      Pages: 1685 - 1686
      Keywords: Free Research Articles
      PubDate: 2017-10-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-08-798546
      Issue No: Vol. 130, No. 15 (2017)
  • RUNX1 in T-ALL: tumor suppressive or oncogenic'
    • Authors: Sanda; T.
      Pages: 1686 - 1688
      Keywords: Free Research Articles
      PubDate: 2017-10-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-08-802181
      Issue No: Vol. 130, No. 15 (2017)
  • Twins actin differently
    • Authors: Li; R.
      Pages: 1688 - 1689
      Keywords: Free Research Articles
      PubDate: 2017-10-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-08-799767
      Issue No: Vol. 130, No. 15 (2017)
  • Impacting inhibitor development in hemophilia A
    • Authors: Konkle; B. A.
      Pages: 1689 - 1690
      Keywords: Free Research Articles
      PubDate: 2017-10-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-08-800763
      Issue No: Vol. 130, No. 15 (2017)
  • Vorinostat is victorious in GVHD prevention
    • Authors: Holtan, S. G; Weisdorf, D. J.
      Pages: 1690 - 1691
      Keywords: Free Research Articles
      PubDate: 2017-10-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-08-802249
      Issue No: Vol. 130, No. 15 (2017)
  • Inflammation: a key regulator of hematopoietic stem cell fate in health
           and disease
    • Authors: Pietras; E. M.
      Pages: 1693 - 1698
      Abstract: Hematopoietic stem cells (HSCs) are responsible for lifelong production of blood cells. At the same time, they must respond rapidly to acute needs such as infection or injury. Significant interest has emerged in how inflammation regulates HSC fate and how it affects the long-term functionality of HSCs and the blood system as a whole. Here we detail recent advances and unanswered questions at the intersection between inflammation and HSC biology in the contexts of development, aging, and hematological malignancy.
      Keywords: Hematopoiesis and Stem Cells, Myeloid Neoplasia, Blood Spotlight
      PubDate: 2017-10-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-06-780882
      Issue No: Vol. 130, No. 15 (2017)
  • Racial and ethnic disparities in hematologic malignancies
    • Authors: Kirtane, K; Lee, S. J.
      Pages: 1699 - 1705
      Abstract: Racial and ethnic disparities in patients with solid malignancies have been well documented. Less is known about these disparities in patients with hematologic malignancies. With the advent of novel chemotherapeutics and targeted molecular, cellular, and immunologic therapies, it is important to identify differences in care that may lead to disparate outcomes. This review provides a critical appraisal of the empirical research on racial and ethnic disparities in incidence, survival, and outcomes in patients with hematologic malignancies. The review focuses on patients with acute myeloid leukemia, acute lymphocytic leukemia, multiple myeloma, non-Hodgkin lymphoma, Hodgkin lymphoma, myeloproliferative neoplasms, and myelodysplastic syndrome. The review discusses possible causes of racial and ethnic disparities and also considers future directions for studies to help decrease disparities.
      Keywords: Myeloid Neoplasia, Lymphoid Neoplasia, Review Articles, Clinical Trials and Observations
      PubDate: 2017-10-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-04-778225
      Issue No: Vol. 130, No. 15 (2017)
  • Management of rivaroxaban- or apixaban-associated major bleeding with
           prothrombin complex concentrates: a cohort study
    • Authors: Majeed, A; Agren, A, Holmström, M, Bruzelius, M, Chaireti, R, Odeberg, J, Hempel, E.-L, Magnusson, M, Frisk, T, Schulman, S.
      Pages: 1706 - 1712
      Abstract: There is uncertainty regarding the effectiveness and occurrence of thromboembolic events in patients treated with prothrombin complex concentrates (PCCs) for the management of major bleeding events (MBEs) on rivaroxaban or apixaban. We investigated the effectiveness of PCCs given for the management of MBEs in patients on rivaroxaban or apixaban. Between 1 January 2014 and 1 October 2016, we prospectively included patients on rivaroxaban or apixaban treated with PCCs for the management of MBEs. The effectiveness of PCCs was assessed by using the International Society of Thrombosis and Hemostasis Scientific and Standardization Subcommittee criteria for the assessment of the effectiveness of major bleeding management. The safety outcomes were thromboembolic events and all-cause mortality within 30 days after treatment with PCCs. A total of 84 patients received PCCs for the reversal of rivaroxaban or apixaban due to a MBE. PCCs were given at a median (interquartile range) dose of 2000 IU (1500-2000 IU). Intracranial hemorrhage (ICH) was the most common site of bleeding requiring reversal (n = 59; 70.2%), followed by gastrointestinal bleeding in 13 (15.5%) patients. Management with PCCs was assessed as effective in 58 (69.1%) patients and ineffective in 26 (30.9%) patients. Most patients with ineffective hemostasis with PCCs had ICH (n = 16; 61.5%). Two patients developed an ischemic stroke, occurring 5 and 10 days after treatment with PCC. Twenty-seven (32%) patients died within 30 days after a MBE. The administration of PCCs for the management of MBEs associated with rivaroxaban or apixaban is effective in most cases and is associated with a low risk of thromboembolism. Our findings are limited by the absence of a control group in the study.
      Keywords: Free Research Articles, Thrombosis and Hemostasis, Clinical Trials and Observations
      PubDate: 2017-10-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-05-782060
      Issue No: Vol. 130, No. 15 (2017)
  • Dendritic cell vaccination as postremission treatment to prevent or delay
           relapse in acute myeloid leukemia
    • Authors: Anguille, S; Van de Velde, A. L, Smits, E. L, Van Tendeloo, V. F, Juliusson, G, Cools, N, Nijs, G, Stein, B, Lion, E, Van Driessche, A, Vandenbosch, I, Verlinden, A, Gadisseur, A. P, Schroyens, W. A, Muylle, L, Vermeulen, K, Maes, M.-B, Deiteren, K, Malfait, R, Gostick, E, Lammens, M, Couttenye, M. M, Jorens, P, Goossens, H, Price, D. A, Ladell, K, Oka, Y, Fujiki, F, Oji, Y, Sugiyama, H, Berneman, Z. N.
      Pages: 1713 - 1721
      Abstract: Relapse is a major problem in acute myeloid leukemia (AML) and adversely affects survival. In this phase 2 study, we investigated the effect of vaccination with dendritic cells (DCs) electroporated with Wilms’ tumor 1 (WT1) messenger RNA (mRNA) as postremission treatment in 30 patients with AML at very high risk of relapse. There was a demonstrable antileukemic response in 13 patients. Nine patients achieved molecular remission as demonstrated by normalization of WT1 transcript levels, 5 of which were sustained after a median follow-up of 109.4 months. Disease stabilization was achieved in 4 other patients. Five-year overall survival (OS) was higher in responders than in nonresponders (53.8% vs 25.0%; P = .01). In patients receiving DCs in first complete remission (CR1), there was a vaccine-induced relapse reduction rate of 25%, and 5-year relapse-free survival was higher in responders than in nonresponders (50% vs 7.7%; P < .0001). In patients age ≤65 and>65 years who received DCs in CR1, 5-year OS was 69.2% and 30.8% respectively, as compared with 51.7% and 18% in the Swedish Acute Leukemia Registry. Long-term clinical response was correlated with increased circulating frequencies of polyepitope WT1-specific CD8+ T cells. Long-term OS was correlated with interferon-+ and tumor necrosis factor-α+ WT1-specific responses in delayed-type hypersensitivity-infiltrating CD8+ T lymphocytes. In conclusion, vaccination of patients with AML with WT1 mRNA-electroporated DCs can be an effective strategy to prevent or delay relapse after standard chemotherapy, translating into improved OS rates, which are correlated with the induction of WT1-specific CD8+ T-cell response. This trial was registered at as #NCT00965224.
      Keywords: Immunobiology and Immunotherapy, Myeloid Neoplasia, Clinical Trials and Observations
      PubDate: 2017-10-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-04-780155
      Issue No: Vol. 130, No. 15 (2017)
  • RUNX1 is required for oncogenic Myb and Myc enhancer activity in T-cell
           acute lymphoblastic leukemia
    • Authors: Choi, A; Illendula, A, Pulikkan, J. A, Roderick, J. E, Tesell, J, Yu, J, Hermance, N, Zhu, L. J, Castilla, L. H, Bushweller, J. H, Kelliher, M. A.
      Pages: 1722 - 1733
      Abstract: The gene encoding the RUNX1 transcription factor is mutated in a subset of T-cell acute lymphoblastic leukemia (T-ALL) patients, and RUNX1 mutations are associated with a poor prognosis. These mutations cluster in the DNA-binding Runt domain and are thought to represent loss-of-function mutations, indicating that RUNX1 suppresses T-cell transformation. RUNX1 has been proposed to have tumor suppressor roles in T-cell leukemia homeobox 1/3–transformed human T-ALL cell lines and NOTCH1 T-ALL mouse models. Yet, retroviral insertional mutagenesis screens identify RUNX genes as collaborating oncogenes in MYC-driven leukemia mouse models. To elucidate RUNX1 function(s) in leukemogenesis, we generated Tal1/Lmo2/Rosa26-CreERT2Runx1f/f mice and examined leukemia progression in the presence of vehicle or tamoxifen. We found that Runx1 deletion inhibits mouse leukemic growth in vivo and that RUNX silencing in human T-ALL cells triggers apoptosis. We demonstrate that a small molecule inhibitor, designed to interfere with CBFβ binding to RUNX proteins, impairs the growth of human T-ALL cell lines and primary patient samples. We demonstrate that a RUNX1 deficiency alters the expression of a crucial subset of TAL1- and NOTCH1-regulated genes, including the MYB and MYC oncogenes, respectively. These studies provide genetic and pharmacologic evidence that RUNX1 has oncogenic roles and reveal RUNX1 as a novel therapeutic target in T-ALL.
      Keywords: Lymphoid Neoplasia
      PubDate: 2017-10-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-03-775536
      Issue No: Vol. 130, No. 15 (2017)
  • NOX5 and p22phox are 2 novel regulators of human monocytic differentiation
           into dendritic cells
    • Authors: Marzaioli, V; Hurtado-Nedelec, M, Pintard, C, Tlili, A, Marie, J.-C, Monteiro, R. C, Gougerot-Pocidalo, M.-A, Dang, P. M.-C, El-Benna, J.
      Pages: 1734 - 1745
      Abstract: Dendritic cells (DCs) are a heterogeneous population of professional antigen-presenting cells and are key cells of the immune system, acquiring different phenotypes in accordance with their localization during the immune response. A subset of inflammatory DCs is derived from circulating monocytes (Mo) and has a key role in inflammation and infection. The pathways controlling Mo-DC differentiation are not fully understood. Our objective was to investigate the possible role of nicotinamide adenine dinucleotide phosphate reduced form oxidases (NOXs) in Mo-DC differentiation. In this study, we revealed that Mo-DC differentiation was inhibited by NOX inhibitors and reactive oxygen species scavengers. We show that the Mo-DC differentiation was dependent on p22phox, and not on gp91phox/NOX2, as shown by the reduced Mo-DC differentiation observed in chronic granulomatous disease patients lacking p22phox. Moreover, we revealed that NOX5 expression was strongly increased during Mo-DC differentiation, but not during Mo-macrophage differentiation. NOX5 was expressed in circulating myeloid DC, and at a lower level in plasmacytoid DC. Interestingly, NOX5 was localized at the outer membrane of the mitochondria and interacted with p22phox in Mo-DC. Selective inhibitors and small interfering RNAs for NOX5 indicated that NOX5 controlled Mo-DC differentiation by regulating the JAK/STAT/MAPK and NFB pathways. These data demonstrate that the NOX5-p22phox complex drives Mo-DC differentiation, and thus could be critical for immunity and inflammation.
      Keywords: Immunobiology and Immunotherapy, Phagocytes, Granulocytes, and Myelopoiesis
      PubDate: 2017-10-12T09:00:28-07:00
      DOI: 10.1182/blood-2016-10-746347
      Issue No: Vol. 130, No. 15 (2017)
  • Twinfilin 2a regulates platelet reactivity and turnover in mice
    • Authors: Stritt, S; Beck, S, Becker, I. C, Vögtle, T, Hakala, M, Heinze, K. G, Du, X, Bender, M, Braun, A, Lappalainen, P, Nieswandt, B.
      Pages: 1746 - 1756
      Abstract: Regulated reorganization of the actin cytoskeleton is a prerequisite for proper platelet production and function. Consequently, defects in proteins controlling actin dynamics have been associated with platelet disorders in humans and mice. Twinfilin 2a (Twf2a) is a small actin-binding protein that inhibits actin filament assembly by sequestering actin monomers and capping filament barbed ends. Moreover, Twf2a binds heterodimeric capping proteins, but the role of this interaction in cytoskeletal dynamics has remained elusive. Even though Twf2a has pronounced effects on actin dynamics in vitro, only little is known about its function in vivo. Here, we report that constitutive Twf2a-deficient mice (Twf2a–/–) display mild macrothrombocytopenia due to a markedly accelerated platelet clearance in the spleen. Twf2a–/– platelets showed enhanced integrin activation and α-granule release in response to stimulation of (hem) immunoreceptor tyrosine-based activation motif (ITAM) and G-protein–coupled receptors, increased adhesion and aggregate formation on collagen I under flow, and accelerated clot retraction and spreading on fibrinogen. In vivo, Twf2a deficiency resulted in shortened tail bleeding times and faster occlusive arterial thrombus formation. The hyperreactivity of Twf2a–/– platelets was attributed to enhanced actin dynamics, characterized by an increased activity of n-cofilin and profilin 1, leading to a thickened cortical cytoskeleton and hence sustained integrin activation by limiting calpain-mediated integrin inactivation. In summary, our results reveal the first in vivo functions of mammalian Twf2a and demonstrate that Twf2a-controlled actin rearrangements dampen platelet activation responses in a n-cofilin– and profilin 1–dependent manner, thereby indirectly regulating platelet reactivity and half-life in mice.
      Keywords: Platelets and Thrombopoiesis, Thrombosis and Hemostasis
      PubDate: 2017-10-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-02-770768
      Issue No: Vol. 130, No. 15 (2017)
  • Genetic risk stratification to reduce inhibitor development in the early
           treatment of hemophilia A: a SIPPET analysis
    • Authors: Rosendaal, F. R; Palla, R, Garagiola, I, Mannucci, P. M, Peyvandi, F, for the SIPPET Study Group
      Pages: 1757 - 1759
      Abstract: A recent randomized trial, the Survey of Inhibitors in Plasma-Product Exposed Toddlers (SIPPET), showed a higher risk of inhibitor development with recombinant factor VIII (rFVIII) than plasma-derived concentrates (pdFVIII). We investigated whether risk stratification by F8 mutation identifies patients who do not suffer this deleterious effect of rFVIII. Among 235 randomized patients with severe hemophilia A previously untreated with FVIII concentrate, 197 with null mutations were classified as high risk and 38 with non-null mutations were classified as low risk. With pdFVIII, no inhibitors occurred in those with low genetic risk, whereas high-risk patients had a cumulative incidence of 31%. The risk among low- and high-risk patients did not differ much when they were treated with rFVIII (43% and 47%, respectively). This implies that patients with low genetic risk suffer disproportionate harm when treated with rFVIII (risk increment 43%), as also shown by the number needed to harm with rFVIII, which was 6.3 for genetically high-risk patients and only 2.3 for low-risk patients. Risk stratification by F8 mutation does not identify patients who can be safely treated with rFVIII, as relates to immunogenicity. This trial was registered at the European Clinical Trials Database (EudraCT) as #2009-011186-88 and at as #NCT01064284.
      Keywords: Thrombosis and Hemostasis, Brief Reports, Clinical Trials and Observations
      PubDate: 2017-10-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-06-791756
      Issue No: Vol. 130, No. 15 (2017)
  • Vorinostat plus tacrolimus/methotrexate to prevent GVHD after
           myeloablative conditioning, unrelated donor HCT
    • Authors: Choi, S. W; Braun, T, Henig, I, Gatza, E, Magenau, J, Parkin, B, Pawarode, A, Riwes, M, Yanik, G, Dinarello, C. A, Reddy, P.
      Pages: 1760 - 1767
      Abstract: The oral histone deacetylase (HDAC) inhibitor (vorinostat) is safe and results in low incidence of acute graft-versus-host disease (GVHD) after reduced-intensity conditioning, related donor hematopoietic cell transplantation (HCT). However, its safety and efficacy in preventing acute GVHD in settings of heightened clinical risk that use myeloablative conditioning, unrelated donor (URD), and methotrexate are not known. We conducted a prospective, phase 2 study in this higher-risk setting. We enrolled 37 patients to provide 80% power to detect a significant difference in grade 2 to 4 acute GVHD of 50% compared with a reduction in target to 28%. Eligibility included adults with a hematological malignancy to receive myeloablative HCT from an available 8/8-HLA matched URD. Patients received GVHD prophylaxis with tacrolimus and methotrexate. Vorinostat (100 mg twice daily) was started on day –10 and continued through day +100 post-HCT. Median age was 56 years (range, 18-69 years), and 95% had acute myelogenous leukemia or high-risk myelodysplastic syndrome. Vorinostat was safe and tolerable. The cumulative incidence of grade 2 to 4 acute GVHD at day 100 was 22%, and for grade 3 to 4 it was 8%. The cumulative incidence of chronic GVHD was 29%; relapse, nonrelapse mortality, GVHD-free relapse-free survival, and overall survival at 1 year were 19%, 16%, 47%, and 76%, respectively. Correlative analyses showed enhanced histone (H3) acetylation in peripheral blood mononuclear cells and reduced interleukin 6 (P = .028) and GVHD biomarkers (Reg3, P = .041; ST2, P = .002) at day 30 post-HCT in vorinostat-treated subjects compared with similarly treated patients who did not receive vorinostat. Vorinostat for GVHD prevention is an effective strategy that should be confirmed in a randomized phase 3 study. This trial was registered at as #NCT01790568.
      Keywords: Transplantation, Free Research Articles, Clinical Trials and Observations
      PubDate: 2017-10-12T09:00:29-07:00
      DOI: 10.1182/blood-2017-06-790469
      Issue No: Vol. 130, No. 15 (2017)
  • Ruxolitinib for essential thrombocythemia refractory to or intolerant of
           hydroxyurea: long-term phase 2 study results
    • Authors: Verstovsek, S; Passamonti, F, Rambaldi, A, Barosi, G, Rumi, E, Gattoni, E, Pieri, L, Zhen, H, Granier, M, Assad, A, Cazzola, M, Kantarjian, H. M, Barbui, T, Vannucchi, A. M.
      Pages: 1768 - 1771
      Keywords: Free Research Articles, Myeloid Neoplasia, Clinical Trials and Observations
      PubDate: 2017-10-12T09:00:29-07:00
      DOI: 10.1182/blood-2017-02-765032
      Issue No: Vol. 130, No. 15 (2017)
  • Long-term results of a phase 2 study of rituximab and bendamustine for
           mucosa-associated lymphoid tissue lymphoma
    • Authors: Salar, A; Domingo-Domenech, E, Panizo, C, Nicolas, C, Bargay, J, Muntanola, A, Canales, M, Bello, J. L, Sancho, J. M, Tomas, J. F, Rodriguez, M. J, Penalver, J, Grande, C, Sanchez-Blanco, J. J, Palomera, L, Arranz, R, Conde, E, Garcia, M, Garcia, J. F, Caballero, D, Montalban, C.
      Pages: 1772 - 1774
      Keywords: Free Research Articles, Lymphoid Neoplasia, Clinical Trials and Observations
      PubDate: 2017-10-12T09:00:29-07:00
      DOI: 10.1182/blood-2017-07-795302
      Issue No: Vol. 130, No. 15 (2017)
  • AML with myelodysplasia-related changes masquerades as acute panmyelosis
           with myelofibrosis
    • Authors: Xu; Z.
      Pages: 1775 - 1775
      Keywords: Free Research Articles, BloodWork, Myeloid Neoplasia
      PubDate: 2017-10-12T09:00:29-07:00
      DOI: 10.1182/blood-2017-06-793554
      Issue No: Vol. 130, No. 15 (2017)
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