Blood (BLOOD)

Publisher: American Society of Hematology, American Society of Hematology

Journal description

Blood, The Journal of The American Society of Hematology is published 25 times (in two volumes) per year by The American Society of Hematology (ASH).

Current impact factor: 10.45

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 10.452
2013 Impact Factor 9.775
2012 Impact Factor 9.06
2011 Impact Factor 9.898
2010 Impact Factor 10.558
2009 Impact Factor 10.555
2008 Impact Factor 10.432
2007 Impact Factor 10.896
2006 Impact Factor 10.37
2005 Impact Factor 10.131
2004 Impact Factor 9.782
2003 Impact Factor 10.12
2002 Impact Factor 9.631
2001 Impact Factor 9.273
2000 Impact Factor 8.977
1999 Impact Factor 8.782
1998 Impact Factor 8.372
1997 Impact Factor 9.507
1996 Impact Factor 9.745
1995 Impact Factor 8.569
1994 Impact Factor 8.279
1993 Impact Factor 8.12
1992 Impact Factor 8.061

Impact factor over time

Impact factor

Additional details

5-year impact 9.57
Cited half-life 7.10
Immediacy index 2.42
Eigenfactor 0.37
Article influence 3.63
Website Blood website
Other titles Blood
ISSN 0006-4971
OCLC 1536582
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

American Society of Hematology

  • Pre-print
    • Author cannot archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Cannot archive until publication
    • On author's personal website and departmental website
    • Must link to publisher version
    • NIH Authors articles will be automatically submitted to PubMed Central after 12 months
  • Classification

Publications in this journal

  • Mark T S Williams · Yasar M Yousafzai · Alex Elder · Klaus Rehe · Simon Bomken · Liron Frishman-Levy · Sigal Tavor · Paul Sinclair · Katie Dormon · Dino Masic · [...] · Victoria J Weston · Pamela Kearns · Helen Blair · Lisa J Russell · Olaf Heidenreich · Julie A E Irving · Shai Izraeli · Josef Vormoor · Gerard J Graham · Christina Halsey ·
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    ABSTRACT: Prevention of central nervous system (CNS) relapse is critical for cure of childhood B-cell precursor acute lymphoblastic leukaemia (BCP-ALL). Despite this, mechanisms of CNS infiltration are poorly understood and the timing, frequency and properties of BCP-ALL blasts entering the CNS compartment are unknown. We investigated the CNS-engrafting potential of BCP-ALL cells xenotransplanted into immunodeficient NOD.Cg-Prkdc(scid)Il2rg(tm1Wjl)/SzJ mice. CNS engraftment was seen in 23/29 diagnostic samples (79%), 2/2 from patients with overt CNS disease and 21/27 (78%) from patients thought to be CNS-negative by diagnostic lumbar puncture. Histological findings mimic human pathology and demonstrate that leukaemic cells primarily transit the blood-cerebrospinal-fluid barrier sitting in close proximity to the dural sinuses - the site of recently discovered CNS lymphatics. Retrieval of blasts from the CNS showed no evidence for chemokine receptor-mediated selective trafficking. The high frequency of infiltration and lack of selective trafficking led us to postulate that CNS tropism is a generic property of leukaemic cells. To test this we performed serial dilution experiments, CNS engraftment was seen in 5/6 mice following transplantation of as few as 10 leukaemic cells. Finally, clonal tracking techniques confirmed the polyclonal nature of CNS infiltrating cells with multiple clones engrafting in both the CNS and periphery. Overall, these findings suggest that sub-clinical seeding of the CNS is likely to be present in the majority of BCP-ALL patients at original diagnosis and efforts to prevent CNS relapse should concentrate on augmenting effective eradication of disease from this site, rather than targeting entry mechanisms.
    No preview · Article · Feb 2016 · Blood
  • Maria I Mascarenhas · Wendi A Bacon · Chrysa Kapeni · Simon R Fitch · Gillian Kimber · S W Priscilla Cheng · Juan Li · Anthony R Green · Katrin Ottersbach
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    ABSTRACT: The regulation of hematopoietic stem cell (HSC) emergence during development provides important information about the basic mechanisms of blood stem cell generation, expansion and migration. We set out to investigate the role that cytokine signaling pathways play in these early processes and show here that the two cytokines interleukin 3 and thrombopoietin have the ability to expand hematopoietic stem and progenitor numbers by regulating their survival and proliferation. For this, they differentially employ the Jak2 and Pi3k signaling pathways, with Jak2 mainly relaying the pro-proliferation signaling, while Pi3k mediates the survival signal. Furthermore, using Jak2-deficient embryos, we demonstrate that Jak2 is crucially required for the function of the first HSCs, while progenitors are less dependent on Jak2. The JAK2V617F mutation, which renders JAK2 constitutively active and which has been linked to myeloproliferative neoplasms, was recently shown to compromise adult HSC function, negatively affecting their repopulation and self-renewal ability, partly through the accumulation of JAK2V617F-induced DNA damage. We report here that nascent HSCs are resistant to the JAK2V617F mutation and show no decrease in repopulation or self-renewal and no increase in DNA damage, even in the presence of two mutant copies. More importantly, this unique property of embryonic HSCs is stably maintained through at least one round of successive transplantations. In summary, our dissection of cytokine signaling in embryonic HSCs has uncovered unique properties of these cells that are of clinical importance.
    No preview · Article · Feb 2016 · Blood
  • Marialaura Bonaccio · Augusto Di Castelnuovo · Simona Costanzo · Amalia De Curtis · Maria Benedetta Donati · Chiara Cerletti · Giovanni de Gaetano · Licia Iacoviello

    No preview · Article · Feb 2016 · Blood
  • Fernando E Sepulveda · Alexandrine Garrigue · Sophia Maschalidi · Meriem Garfa-Traore · Gaël Ménasché · Alain Fischer · Genevieve de Saint Basile
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    ABSTRACT: Hemophagocytic lymphohistiocytosis (HLH) consists in a life-threatening hyperinflammatory disease. Inherited forms of HLH are caused by biallelic mutations in several effectors of granule-dependent lymphocyte-mediated cytotoxicity. A small proportion of patients with a so-called "secondary" form of HLH, which develops in the aftermath of infection, autoimmunity or cancer, carry a monoallelic mutation in one or more HLH-associated genes. Although this observation suggests that HLH may have a polygenic mode of inheritance, the latter is very difficult to prove in humans. In order to determine whether the accumulation of partial genetic defects in lymphocyte-mediated cytotoxicity can contribute to the development of HLH, we generated mice that were doubly or triply heterozygous for mutations in HLH-associated genes, those coding for perforin, Rab27a and syntaxin-11. We found that the accumulation of monoallelic mutations did indeed increase the risk of developing HLH immunopathology after LCMV infection. In mechanistic terms, the accumulation of heterozygous mutations in the two degranulation genes Rab27a and syntaxin-11, impaired the dynamics and secretion of cytotoxic granules at the immune synapse of T lymphocytes. In addition, the accumulation of heterozygous mutations within the three genes impaired NK lymphocyte cytotoxicity in vivo. The genetic defects can be ranked in terms of the severity of the resulting HLH manifestations. Our results form the basis of a polygenic model of the occurrence of secondary HLH.
    No preview · Article · Feb 2016 · Blood
  • Yashodhara Dasgupta · Mateusz Koptyra · Grazyna Hoser · Kanchan Kantekure · Darshan Roy · Barbara Gornicka · Margaret Nieborowska-Skorska · Elisabeth Bolton-Gillespie · Sabine Cerny-Reiterer · M. Muschen · Peter Valent · Mariusz A Wasik · Christine Richardson · Oliver Hantschel · Heiko van der Kuip · Tomasz Stoklosa · Tomasz Skorski
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    ABSTRACT: Leukemias expressing constitutively activated mutants of ABL1 tyrosine kinase (BCR-ABL1, TEL-ABL1, NUP214-ABL1) usually contain at least one normal ABL1 allele. Since oncogenic and normal ABL1 kinases may exert opposite effects on cell behavior we examined the role of normal ABL1 in leukemias induced by oncogenic ABL1 kinases. BCR-ABL1-Abl1-/- cells generated highly aggressive chronic myeloid leukemia-blast phase (CML-BP)-like disease in mice compared to less malignant CML-chronic phase (CML-CP)-like disease from BCR-ABL1-Abl1+/+ cells. Additionally, loss of ABL1 stimulated proliferation and expansion of BCR-ABL1 murine leukemia stem cells, arrested myeloid differentiation, inhibited genotoxic stress-induced apoptosis, and facilitated accumulation of chromosomal aberrations. Conversely, allosteric stimulation of ABL1 kinase activity enhanced anti-leukemia effect of ABL1 tyrosine kinase inhibitors (imatinib and ponatinib) in human and murine leukemias expressing BCR-ABL1, TEL-ABL1 and NUP214-ABL1. Therefore, we postulate that normal ABL1 kinase behaves like a tumor suppressor and therapeutic target in leukemias expressing oncogenic forms of the kinase.
    No preview · Article · Feb 2016 · Blood
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    ABSTRACT: Von Willebrand disease (VWD) is the most common inherited bleeding disorder, and type 1 VWD is the most common VWD variant. Despite its frequency, diagnosis of type 1 VWD remains the subject of much debate. In order to study the spectrum of type 1 VWD in the United States, the Zimmerman Program enrolled 482 subjects with a previous diagnosis of type 1 VWD without stringent laboratory diagnostic criteria. VWF laboratory testing and full length VWF gene sequencing were performed for all index cases and healthy control subjects in a central laboratory. Bleeding phenotype was characterized using the ISTH Bleeding Assessment Tool. At study entry, 64% of subjects had VWF:Ag or VWF:RCo below the lower limit of normal, while 36% had normal VWF levels. VWF sequence variations were most frequent in subjects with VWF:Ag < 30 IU/dL (82%) while subjects with type 1 VWD and VWF:Ag ≥ 30 IU/dL had an intermediate frequency of variants (44%). Subjects whose VWF testing was normal at study entry had a similar rate of sequence variations as the healthy controls at 14% of subjects. All subjects with severe type 1 VWD and VWF:Ag ≤ 5 IU/dL had an abnormal bleeding score, but otherwise bleeding score did not correlate with VWF:Ag level. Subjects with a historical diagnosis of type 1 VWD had similar rates of abnormal bleeding scores compared to subjects with low VWF levels at study entry. Type 1 VWD in the United States is highly variable, and bleeding symptoms are frequent in this population.
    No preview · Article · Feb 2016 · Blood
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    ABSTRACT: Severe Plasmodium falciparum malaria remains a leading cause of mortality, particularly in sub-Saharan Africa where it accounts for up to 1 million deaths per annum. In spite of the significant mortality and morbidity associated with cerebral malaria (CM), the molecular mechanisms involved in the pathophysiology of severe malaria remain surprisingly poorly understood. Previous studies have demonstrated that sequestration of P. falciparum-infected erythrocytes within the microvasculature of the brain plays a key role in the development of CM. In addition, there is convincing evidence that both EC activation and platelets play critical roles in the modulating the pathogenesis of severe P. falciparum malaria. In this review, we provide an overview of recent studies that have identified novel roles through which haemostatic dysfunction may directly influence malaria pathogenesis In particular, we focus on emerging data suggesting that von Willebrand factor, coagulation cascade activation and dysfunction of the protein C pathway may be of specific importance in this context. These collective insights underscore a growing appreciation of the important, but poorly understood, role of haemostatic dysfunction in malaria progression and importantly, illuminate potential approaches for novel therapeutic strategies. Given that the mortality rate associated with CM remains in the order of 20% despite the availability of effective anti-malarial therapy, development of adjunctive therapies that can attenuate CM progression clearly represents a major unmet need. These emerging data are thus not of only of basic scientific interest, but also of direct clinical significance.
    No preview · Article · Feb 2016 · Blood
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    ABSTRACT: Stroke risk in sickle-cell-anemia (SCA) is predicted by high transcranial Doppler (TCD) velocities and prevented by chronic transfusions. Nevertheless, chronic transfusions are associated with severe side effects, such as iron overload. We present here the long-term follow-up of SCA-children from the newborn-CHIC-Créteil-cohort (1992-2012), detected at risk by TCD and placed on chronic transfusions. Patients with normalized-velocities and no persistent stenosis were treated with hydroxyurea, which had been shown to decrease anemia, and hemolytic rate, risk-factors for abnormal-TCD. They were followed with trimestrial Doppler and transfusions re-started immediately in case of reversion to abnormal-velocities. Patients with a genoidentical donor underwent transplantation. Abnormal-TCD (TAMMV≥200cm/sec) was detected in 92 SCA-children, at a mean age of 3.7 years/range:1.3-8.3. With a mean follow-up of 6.1 years, no stroke occurred post-transfusion. Normalization of velocities (TAMMV<170cm/sec) was observed in 83.5% of patients. Stenosis, present in 27.5% of patients, was associated with the risk of non-TCD-normalization (HR=2.6,95%CI:1.5-4,p=0.001). Switch from transfusions to hydroxyurea was prescribed to 45 patients for a mean follow-up of 3.4 years. Reversion, predicted by baseline reticulocyte count ≥400×10(9)/L (HR=6.3,95%CI:1.8-21.7,p=0.001), occurred in 13/45 (28.9%) at the mean age of 7.1 years/range:4.3-9.5. Transplantation, performed in 24 patients, allowed transfusions to be safely stopped in all patients and velocities to be normalized in 4 patients who still had abnormal-velocities on transfusions. This long-term cohort study shows that transfusions can be stopped not only in transplanted patients, but also in a subset of patients switched to hydroxyurea, provided trimestrial Doppler follow-up and immediately re-starting transfusions in case of reversion.
    No preview · Article · Feb 2016 · Blood
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    ABSTRACT: Two classes of novel agents i.e., NAE (NEDD8-activating enzyme) and HDAC (histone deacetylase) inhibitors have shown single-agent activity in AML/MDS. Here we examined mechanisms underlying interactions between the NAE inhibitor pevonedistat (MLN4924) and the approved HDAC inhibitor belinostat in AML/MDS cells. MLN4924/belinostat co-administration synergistically induced AML cell apoptosis (~ 20% individually; 60-90% combined; CI values <1.0) with or without p53 deficiency or FLT3-ITD, while p53 shRNA knock-down or enforced FLT3-ITD expression significantly sensitized cells to the regimen (P < 0.05). MLN4924 blocked belinostat-induced anti-apoptotic gene expression through NF-κB inactivation. Each agent up-regulated Bim, and Bim knock-down significantly attenuated apoptosis. Microarrays revealed distinct DNA damage response (DDR) genetic profiles between individual versus combined MLN4924/belinostat exposure. Whereas belinostat abrogated the MLN4924-activated intra-S checkpoint through Chk1 and Wee1 inhibition/down-regulation, co-treatment down-regulated multiple HR and NHEJ repair proteins, triggering robust DSBs, chromatin pulverization, and apoptosis. Consistently, Chk1 or Wee1 shRNA knockdown significantly sensitized AML cells to MLN4924. MLN4924/belinostat displayed activity against primary AML or MDS cells, including those carrying NGS-defined poor-prognostic cancer hotspot mutations, and CD34(+)/CD38(-)/CD123(+) populations, but not normal CD34(+) progenitors. Finally, combined treatment markedly reduced tumor burden and significantly prolonged animal survival (median survival 205 vs 106 days; P < 0.0001) in both s.c. and i.v. AML xenograft models with negligible toxicity, accompanied by pharmacodynamic effects observed in vitro. Collectively, these findings argue that MLN4924 and belinostat interact synergistically by reciprocally disabling the DDR in AML/MDS cells. This strategy warrants further consideration in AML/MDS, particularly in disease with unfavorable genetic aberrations.
    No preview · Article · Feb 2016 · Blood

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    ABSTRACT: Most physicians believe they practiced personalized medicine prior to the genomics era that followed the sequencing of the human genome. The focus of Personalized Medicine has been primarily genomic medicine, wherein it is hoped that the nucleotide dissimilarities among different individuals would provide clinicians with more precise understanding of physiology, more refined diagnoses, better disease risk assessment, earlier detection and monitoring, and tailored treatments to the individual patient. However, to date the "genomic bench" has not worked itself to the clinical thrombosis bedside. In fact, traditional plasma-based hemostasis-thrombosis laboratory testing, by assessing functional pathways of coagulation, may better help manage venous thrombotic disease than a single DNA variant with a small effect size. There are some new and exciting discoveries in the genetics of platelet reactivity pertaining to atherothrombotic disease. Despite a plethora of genetic/genomic data on platelet reactivity, there is relatively little actionable pharmacogenetic data with anti-platelet agents. Nevertheless, it is crucial for genome wide DNA/RNA sequencing to continue in research settings for causal gene discovery, pharmacogenetic purposes, and gene-gene and gene-environment interactions. The potential of genomics to advance medicine will require integration of personal data that is obtained in the patient history: environmental exposures, diet, social data, etc. Furthermore, without the ritual of obtaining this information, we will have de-personalized medicine to lack the precision needed for the research required to eventually incorporate genomics into routine, optimal and value-added clinical care.
    No preview · Article · Feb 2016 · Blood

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    ABSTRACT: We performed a meta-analysis of randomized controlled trials comparing LMWH versus no LMWH in women with inherited thrombophilia and prior late (≥10 weeks) or recurrent early (<10 weeks) pregnancy loss. Eight trials and 483 patients met our inclusion criteria. There was no significant difference in livebirth rates with the use of LMWH compared to no LMWH (RR 0.81, 95% CI, 0.55 to 1.19, p=0.28), suggesting no benefit of LMWH in preventing recurrent pregnancy loss in women with inherited thrombophilia.
    No preview · Article · Feb 2016 · Blood