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Journal Prestige (SJR): 6.434
Citation Impact (citeScore): 7
Number of Followers: 319  
  Full-text available via subscription Subscription journal
ISSN (Print) 0006-4971 - ISSN (Online) 1528-0020
Published by American Society of Hematology Homepage  [2 journals]
  • von Willebrand factor promotes wound healing
    • Authors: ODonnell, J. S; OSullivan, J. M.
      Pages: 2553 - 2555
      Keywords: Free Research Articles
      PubDate: 2019-06-13T09:00:24-07:00
      DOI: 10.1182/blood.2019001175
      Issue No: Vol. 133, No. 24 (2019)
  • Eltrombopag: wielding a double-edged sword'
    • Authors: Babushok D. V.
      Pages: 2555 - 2556
      Keywords: Free Research Articles
      PubDate: 2019-06-13T09:00:24-07:00
      DOI: 10.1182/blood.2019001327
      Issue No: Vol. 133, No. 24 (2019)
  • B-1 progenitor acute lymphoid leukemia
    • Authors: Yoshimoto M.
      Pages: 2557 - 2558
      Keywords: Free Research Articles
      PubDate: 2019-06-13T09:00:24-07:00
      DOI: 10.1182/blood.2019001249
      Issue No: Vol. 133, No. 24 (2019)
  • The heparin binding domain of von Willebrand factor binds to growth
           factors and promotes angiogenesis in wound healing
    • Authors: Ishihara, J; Ishihara, A, Starke, R. D, Peghaire, C. R, Smith, K. E, McKinnon, T. A. J, Tabata, Y, Sasaki, K, White, M. J. V, Fukunaga, K, Laffan, M. A, Lutolf, M. P, Randi, A. M, Hubbell, J. A.
      Pages: 2559 - 2569
      Abstract: During wound healing, the distribution, availability, and signaling of growth factors (GFs) are orchestrated by their binding to extracellular matrix components in the wound microenvironment. Extracellular matrix proteins have been shown to modulate angiogenesis and promote wound healing through GF binding. The hemostatic protein von Willebrand factor (VWF) released by endothelial cells (ECs) in plasma and in the subendothelial matrix has been shown to regulate angiogenesis; this function is relevant to patients in whom VWF deficiency or dysfunction is associated with vascular malformations. Here, we show that VWF deficiency in mice causes delayed wound healing accompanied by decreased angiogenesis and decreased amounts of angiogenic GFs in the wound. We show that in vitro VWF binds to several GFs, including vascular endothelial growth factor-A (VEGF-A) isoforms and platelet-derived growth factor-BB (PDGF-BB), mainly through the heparin-binding domain (HBD) within the VWF A1 domain. VWF also binds to VEGF-A and fibroblast growth factor-2 (FGF-2) in human plasma and colocalizes with VEGF-A in ECs. Incorporation of the VWF A1 HBD into fibrin matrices enables sequestration and slow release of incorporated GFs. In vivo, VWF A1 HBD-functionalized fibrin matrices increased angiogenesis and GF retention in VWF-deficient mice. Treatment of chronic skin wounds in diabetic mice with VEGF-A165 and PDGF-BB incorporated within VWF A1 HBD-functionalized fibrin matrices accelerated wound healing, with increased angiogenesis and smooth muscle cell proliferation. Therefore, the VWF A1 HBD can function as a GF reservoir, leading to effective angiogenesis and tissue regeneration.
      Keywords: Plenary Papers, Thrombosis and Hemostasis, Vascular Biology
      PubDate: 2019-06-13T09:00:24-07:00
      DOI: 10.1182/blood.2019000510
      Issue No: Vol. 133, No. 24 (2019)
  • Acalabrutinib for mantle cell lymphoma
    • Authors: Witzig, T. E; Inwards, D.
      Pages: 2570 - 2574
      Abstract: Mantle cell lymphoma (MCL) is a unique type of non-Hodgkin lymphoma characterized by the overexpression of cyclin D1. MCL patients typically live for years but experience multiple relapses. Acalabrutinib is a novel second-generation oral Bruton tyrosine kinase inhibitor approved by the US Food and Drug Administration for relapsed MCL based on a clinical trial demonstrating an overall response rate of 81%. It provides a valuable new treatment option for MCL patients and is now being tested upfront.
      Keywords: Lymphoid Neoplasia, Blood Spotlight
      PubDate: 2019-06-13T09:00:24-07:00
      DOI: 10.1182/blood.2019852368
      Issue No: Vol. 133, No. 24 (2019)
  • Treatment optimization and genomic outcomes in refractory severe aplastic
           anemia treated with eltrombopag
    • Authors: Winkler, T; Fan, X, Cooper, J, Desmond, R, Young, D. J, Townsley, D. M, Scheinberg, P, Grasmeder, S, Larochelle, A, Desierto, M, Valdez, J, Lotter, J, Wu, C, Shalhoub, R. N, Calvo, K. R, Young, N. S, Dunbar, C. E.
      Pages: 2575 - 2585
      Abstract: Eltrombopag (EPAG) received approval from the US Food and Drug Administration for the treatment of refractory severe aplastic anemia (rSAA) based on treatment of 43 patients with doses escalating from 50 to 150 mg daily for 12 weeks. Response kinetics suggested that more prolonged administration of EPAG at a dose of 150 mg could speed and improve response rates. We enrolled 40 patients with rSAA in a study of EPAG 150 mg daily, with a primary end point of response at 24 weeks. Twenty (50%) of 40 patients responded at 24 weeks; 5 (25%) of 20 would have been deemed nonresponders at 12 weeks, the end point of the previous study. Fifteen of the 19 responding patients continuing on EPAG had drug discontinued for robust response; 5 of the 15 required EPAG re-initiation for relapse, with all recovering response. To analyze risk of clonal progression, we combined long-term data from the 83 patients with rSAA enrolled in both studies. Evolution to an abnormal karyotype occurred in 16 (19%), most within 6 months of EPAG initiation. Targeted deep sequencing/whole-exome sequencing was performed pre-EPAG and at primary response end point and/or time of clonal evolution or longest follow-up. Cytogenetic evolution did not correlate with mutational status, and overall mutated allele fractions of myeloid cancer genes did not increase on EPAG. In summary, extended administration of EPAG at a dose of 150 mg for 24 weeks rescued responses in some patients with rSAA not responding at 12 weeks. The temporal relationship between clonal evolution and drug exposure suggests that EPAG may promote expansion of dormant preexisting clones with an aberrant karyotype. The studies were registered at as #NCT00922883 and #NCT01891994.
      Keywords: Hematopoiesis and Stem Cells, Clinical Trials and Observations
      PubDate: 2019-06-13T09:00:24-07:00
      DOI: 10.1182/blood.2019000478
      Issue No: Vol. 133, No. 24 (2019)
  • Clinical and immunological features in a cohort of patients with partial
           DiGeorge syndrome followed at a single center
    • Authors: Giardino, G; Radwan, N, Koletsi, P, Morrogh, D. M, Adams, S, Ip, W, Worth, A, Jones, A, Meyer-Parsonson, I, Gaspar, H. B, Gilmour, K, Davies, E. G, Ladomenou, F.
      Pages: 2586 - 2596
      Abstract: DiGeorge syndrome (DGS) is a primary immunodeficiency characterized by various degrees of T-cell deficiency. In partial DGS (pDGS), other risk factors could predispose to recurrent infections, autoimmunity, and allergy. The aim of this study was to assess the effect of different factors in the development of infections, autoimmunity, and/or allergy in patients with pDGS. We studied 467 pDGS patients in follow-up at Great Ormond Street Hospital. Using a multivariate approach, we observed that palatal anomalies represent a risk factor for the development of recurrent otitis media with effusion. Gastroesophageal reflux/dysphagia and asthma/rhinitis represent a risk factor for the development of recurrent upper respiratory tract infections. Allergy and autoimmunity were associated with persistently low immunoglobulin M levels and lymphopenia, respectively. Patients with autoimmunity showed lower levels of CD3+, CD3+CD4+, and naïve CD4+CD45RA+CD27+ T lymphocytes compared with pDGS patients without autoimmunity. We also observed that the physiological age-related decline of the T-cell number was slower in pDGS patients compared with age-matched controls. The age-related recovery of the T-cell number depended on a homeostatic peripheral proliferation of T cells, as suggested by an accelerated decline of the naïve T lymphocytes in pDGS as well as a more skewed T-cell repertoire in older pDGS patients. These evidences suggest that premature CD4+ T-cell aging and lymphopenia induced spontaneous peripheral T-cell proliferation might contribute to the pathogenesis of autoimmunity in patients with pDGS. Infections in these patients represent, in most of the cases, a complication of anatomical or gastroenterological anomalies rather than a feature of the underlying immunodeficiency.
      Keywords: Pediatric Hematology, Immunobiology and Immunotherapy
      PubDate: 2019-06-13T09:00:24-07:00
      DOI: 10.1182/blood.2018885244
      Issue No: Vol. 133, No. 24 (2019)
  • Chronic CD30 signaling in B cells results in lymphomagenesis by driving
           the expansion of plasmablasts and B1 cells
    • Authors: Sperling, S; Fiedler, P, Lechner, M, Pollithy, A, Ehrenberg, S, Schiefer, A.-I, Kenner, L, Feuchtinger, A, Kühn, R, Swinerd, G, Schmidt-Supprian, M, Strobl, L. J, Zimber-Strobl, U.
      Pages: 2597 - 2609
      Abstract: CD30 is expressed on a variety of B-cell lymphomas, such as Hodgkin lymphoma, primary effusion lymphoma, and a diffuse large B-cell lymphoma subgroup. In normal tissues, CD30 is expressed on some activated B and T lymphocytes. However, the physiological function of CD30 signaling and its contribution to the generation of CD30+ lymphomas are still poorly understood. To gain a better understanding of CD30 signaling in B cells, we studied the expression of CD30 in different murine B-cell populations. We show that B1 cells expressed higher levels of CD30 than B2 cells and that CD30 was upregulated in IRF4+ plasmablasts (PBs). Furthermore, we generated and analyzed mice expressing a constitutively active CD30 receptor in B lymphocytes. These mice displayed an increase in B1 cells in the peritoneal cavity (PerC) and secondary lymphoid organs as well as increased numbers of plasma cells (PCs). TI-2 immunization resulted in a further expansion of B1 cells and PCs. We provide evidence that the expanded B1 population in the spleen included a fraction of PBs. CD30 signals seemed to enhance PC differentiation by increasing activation of NF-B and promoting higher levels of phosphorylated STAT3 and STAT6 and nuclear IRF4. In addition, chronic CD30 signaling led to B-cell lymphomagenesis in aged mice. These lymphomas were localized in the spleen and PerC and had a B1-like/plasmablastic phenotype. We conclude that our mouse model mirrors chronic B-cell activation with increased numbers of CD30+ lymphocytes and provides experimental proof that chronic CD30 signaling increases the risk of B-cell lymphomagenesis.
      Keywords: Lymphoid Neoplasia
      PubDate: 2019-06-13T09:00:24-07:00
      DOI: 10.1182/blood.2018880138
      Issue No: Vol. 133, No. 24 (2019)
  • Engineered Bcor mutations lead to acute leukemia of progenitor B-1
           lymphocyte origin in a sensitized background
    • Authors: Yin, M; Chung, Y. J, Lindsley, R. C, Walker, R. L, Zhu, Y. J, Ebert, B. L, Meltzer, P. S, Aplan, P. D.
      Pages: 2610 - 2614
      Abstract: Approximately 10% of NUP98-PHF23 (NP23) mice develop an aggressive acute lymphoblastic leukemia of B-1 lymphocyte progenitor origin (pro-B1 ALL), accompanied by somatic frameshift mutations of the BCL6 interacting corepressor (Bcor) gene, most commonly within a 9-bp "hotspot" in Bcor exon 8. To determine whether experimentally engineered Bcor mutations would lead to pro-B1 ALL, we used clustered, regularly interspaced, short palindromic repeats–associated protein 9 to introduce a Bcor frameshift mutation into NP23 hematopoietic stem and progenitor cells through the use of Bcor small guide RNAs (Bcor sgRNAs). Recipient mice transplanted with NP23 bone marrow or fetal liver cells that had been transduced with a Bcor sgRNA developed pro-B1 ALL, characterized by a B-1 progenitor immunophenotype, clonal Igh gene rearrangement, and Bcor indel mutation, whereas control recipients did not. Similar to a subset of human B-cell precursor ALL, the murine pro-B1 ALL had acquired somatic mutations in Jak kinase genes. JAK inhibitors (ruxolitinib and tofacitinib) inhibited the growth of pro-B1 ALL cell lines established from Bcor sgRNA/NP23 recipients at clinically achievable concentrations (100 nM). Our results demonstrate that Bcor mutations collaborate with NP23 to induce pro-B1 ALL, and that JAK inhibitors are potential therapies for pro-B1 ALL.
      Keywords: Lymphoid Neoplasia, Brief Reports
      PubDate: 2019-06-13T09:00:24-07:00
      DOI: 10.1182/blood.2018864173
      Issue No: Vol. 133, No. 24 (2019)
  • With equal access, African American patients have superior survival
           compared to white patients with multiple myeloma: a VA study
    • Authors: Fillmore, N. R; Yellapragada, S. V, Ifeorah, C, Mehta, A, Cirstea, D, White, P. S, Rivero, G, Zimolzak, A, Pyarajan, S, Do, N, Brophy, M, Munshi, N. C.
      Pages: 2615 - 2618
      Keywords: Multiple Myeloma, Sickle Cell Disease, Red Cells, Iron, and Erythropoiesis, Lymphoid Neoplasia, Clinical Trials and Observations
      PubDate: 2019-06-13T09:00:24-07:00
      DOI: 10.1182/blood.2019000406
      Issue No: Vol. 133, No. 24 (2019)
  • Archeogenetics of F11 p.Cys38Arg: a 5400-year-old mutation identified in
           different southwestern European countries
    • Authors: de la Morena-Barrio, M. E; Salloum-Asfar, S, Esteban, J, de la Morena-Barrio, B, Altisent, C, Martin-Fernandez, L, Gueguen, P, Padilla, J, Minano, A, Parra, R, Vicente, V, Vidal, F, Bauduer, F, Carbonell, P, Corral, J.
      Pages: 2618 - 2622
      Keywords: Thrombosis and Hemostasis
      PubDate: 2019-06-13T09:00:24-07:00
      DOI: 10.1182/blood.2019000055
      Issue No: Vol. 133, No. 24 (2019)
  • HTLV-1-associated adult T-cell leukemia/lymphoma with disseminated
    • Authors: Kwon, R; Duffield, A. S.
      Pages: 2623 - 2623
      Keywords: Free Research Articles, BloodWork, Lymphoid Neoplasia
      PubDate: 2019-06-13T09:00:24-07:00
      DOI: 10.1182/blood.2019000290
      Issue No: Vol. 133, No. 24 (2019)
  • Unusual case of a myelodysplastic syndrome with novel inv(5)(q15q33)
    • Authors: Golden, R. J; Bogusz, A. M.
      Pages: 2624 - 2624
      Keywords: Free Research Articles, BloodWork, Myeloid Neoplasia
      PubDate: 2019-06-13T09:00:24-07:00
      DOI: 10.1182/blood.2019000090
      Issue No: Vol. 133, No. 24 (2019)
  • Go╠łkbuget N, Dombret H, Bonifacio M, et al. Blinatumomab for minimal
           residual disease in adults with B-cell precursor acute lymphoblastic
           leukemia. Blood. 2018;131(14):1522-1531.
    • Pages: 2625 - 2625
      Keywords: Free Research Articles
      PubDate: 2019-06-13T09:00:24-07:00
      DOI: 10.1182/blood.2019001109
      Issue No: Vol. 133, No. 24 (2019)
School of Mathematical and Computer Sciences
Heriot-Watt University
Edinburgh, EH14 4AS, UK
Tel: +00 44 (0)131 4513762
Fax: +00 44 (0)131 4513327
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