Blood Journal Impact Factor & Information

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

2015 Impact Factor Available summer 2016
2014 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

  • Blood 11/2015; 126(22):2440-2442. DOI:10.1182/blood-2015-09-668970

  • Blood 11/2015; 126(22):2439-2440. DOI:10.1182/blood-2015-10-671362

  • Blood 11/2015; 126(22):2522-2522. DOI:10.1182/blood-2015-09-668210
  • [Show abstract] [Hide abstract]
    ABSTRACT: Transplant-associated thrombotic microangiopathy (TMA) occurs frequently after hematopoietic stem cell transplantation (HSCT), and can lead to significant morbidity and mortality. There are no data addressing individual susceptibility to transplant-associated TMA. We performed a hypothesis driven analysis of 17 candidate genes known to play a role in complement activation as part of a prospective study of TMA in HSCT recipients. We examined the functional significance of gene variants using gene expression profiling. Among 77 subjects undergoing genetic testing, 34 had TMA. Sixty five percent of patients with TMA had genetic variants in at least one gene, as compared to 9% of patients without TMA (p<0.0001). Gene variants were increased in subjects with TMA of all races, but non-Caucasians had more variants than Caucasians (2.5 (0-7) vs 0 (0-2), p<0.0001). Variants in ≥3 genes were identified only in non-Caucasians with TMA, and were associated with high mortality (71%). RNAseq analysis of pre-transplant samples showed upregulation of multiple complement pathways in subjects with TMA who had gene variants, including variants predicted as possibly benign by computer algorithm, as compared to those without TMA and without gene variants. Our data reveal important differences in genetic susceptibility to HSCT-associated TMA based on recipient genotype. These data will allow prospective risk assessment and intervention to prevent TMA in highly susceptible transplant recipients. Our findings may explain, at least in part, racial disparities previously reported in transplant recipients and may guide treatment strategies to improve outcomes.
    Blood 11/2015; DOI:10.1182/blood-2015-08-663435
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    ABSTRACT: GLI1 oncogene has been implicated in the pathobiology of several neoplasms including diffuse large B-cell lymphoma (DLBCL). However, mechanisms underlying GLI1 increased activity in DLBCL are poorly characterized. Herein, we demonstrate that IKKβ phosphorylates GLI1 in DLBCL. IKKβ activation increased GLI1 protein levels and transcriptional activity, while IKKβ silencing decreased GLI1 levels and transcriptional activity. TNFα-mediated IKKβ activation impaired GLI1 binding with the E3 ubiquitin ligase-ITCH, leading to decreased K48-linked ubiquitination/degradation of GLI1. We found eight IKKβ-dependent phosphorylation sites that mediate GLI1 stability. Mutating or deleting these residues facilitated GLI1-ITCH interaction and decreased the protective effect of TNFα on GLI1 stability. IKKβ-GLI1 crosstalk is significant as combined inhibition of both molecules resulted in synergistic suppression of DLBCL viability in vivo and in vitro. By linking IKKβ-mediated NF-κB activity with GLI1, we identified a crosstalk between these two pathways that can inform the design of novel therapeutic strategies in DLBCL.
    Blood 11/2015; DOI:10.1182/blood-2015-07-658781
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    ABSTRACT: BCR-ABL1 kinase domain mutations can confer resistance to first- and second-generation tyrosine kinase inhibitors (TKIs) in chronic myeloid leukemia (CML). In pre-clinical studies, clinically achievable concentrations of the third-generation BCR-ABL1 TKI ponatinib inhibit T315I and all other single BCR-ABL1 mutants except T315M, which generates a single amino acid exchange, but requires 2 sequential nucleotide exchanges. Additionally, certain compound mutants (containing ≥2 mutations in cis) confer resistance. Initial analyses based largely on conventional Sanger sequencing (SS) have suggested that the preclinical relationship between BCR-ABL1 mutation status and ponatinib efficacy is generally recapitulated in patients on therapy. Thus far, however, such analyses have been limited by the inability of SS to definitively identify compound mutations or mutations representing less than ~20% of total alleles (referred to as low-level mutations), as well as limited patient follow-up. Here we used next-generation sequencing (NGS) to define the baseline BCR-ABL1 mutation status of 267 heavily pre-treated CP-CML patients from the PACE trial, and used SS to identify clonally dominant mutants that may have developed on ponatinib therapy (30.1-months median follow-up). Durable cytogenetic and molecular responses were observed irrespective of baseline mutation status, and included patients with compound mutations. No single or compound mutation was identified that consistently conferred primary and/or secondary resistance to ponatinib in CP-CML patients. Ponatinib is effective in CP-CML irrespective of baseline mutation status.
    Blood 11/2015; DOI:10.1182/blood-2015-08-660977
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    ABSTRACT: Platelet-driven blood clot contraction (retraction) is thought to promote wound closure and secure hemostasis while preventing vascular occlusion. Notwithstanding its importance, clot contraction remains a poorly understood process, partially due to the lack of methodology to quantify its dynamics and requirements. We used a novel automated optical analyzer to continuously track in vitro changes in the size of contracting clots in whole blood and in variously reconstituted samples. Kinetics of contraction was complemented with dynamic rheometry to characterize the viscoelasticity of contracting clots. This combined approach enabled investigation of the coordinated mechanistic impact of platelets, including non-muscle myosin II, red blood cells, fibrin(ogen), factor XIIIa, and thrombin on the kinetics and mechanics of the contraction process. Clot contraction is comprised of three sequential phases, each characterized by a distinct rate constant. Thrombin, Ca(2+), the integrin αIIbβ3, myosin IIa, factor XIIIa-crosslinking, and platelet count all promote one or more phases of the clot contraction process. In contrast, RBCs impair contraction and reduce elasticity, while increasing the overall contractile stress generated by the platelet-fibrin meshwork. A better understanding of the mechanisms by which blood cells, fibrin(ogen), and platelet-fibrin interactions modulate clot contraction may generate novel approaches to reveal and to manage thrombosis and hemostatic disorders.
    Blood 11/2015; DOI:10.1182/blood-2015-05-647560
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    ABSTRACT: The Sterile-20 kinase MINK1 is involved in many important cellular processes such as growth, cytoskeletal rearrangement, and motility. Here, with MINK1-deficient (MINK1(-/-)) mice, we showed that MINK1 plays an important role in hemostasis and thrombosis via the regulation of platelet functions. In the tail-bleeding assay, MINK1(-/-) mice exhibited a longer bleeding time than wild-type mice (589.0 ± 68.1 s versus 406.6 ± 70.5 s). In a model of ferric chloride-induced mesenteric arteriolar thrombosis, vessel occlusion times were twice as long in MINK1(-/-) mice as in wild-type mice. In an in vitro microfluidic whole-blood perfusion assay, thrombus formation on a collagen matrix under arterial shear conditions was significantly reduced in MINK1(-/-) platelets. Moreover, MINK1(-/-) platelets demonstrated impaired aggregation and secretion in response to low doses of thrombin and collagen. Furthermore, platelet spreading on fibrinogen was largely hampered in MINK1(-/-) platelets. The functional differences of MINK1(-/-) platelets could be attributed to impaired ADP secretion. Signaling events associated with MINK1 appeared to involve ERK, p38, and Akt. Hence, MINK1 may be an important signaling molecule that mediates MAPK signaling and participates in platelet activation and thrombus formation.
    Blood 11/2015; DOI:10.1182/blood-2015-07-659185
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    ABSTRACT: Septic transfusion reactions (STR) resulting from transfusion of bacterially contaminated platelets are a major hazard of platelet transfusion despite recent interventions. Active and passive surveillance for bacterially contaminated platelets were performed over 7-years (2007-2013) by culture of platelet aliquots at time of transfusion and review of reported transfusion reactions. All platelet units had been cultured 24 h after collection and released as negative. Five sets of STR criteria were evaluated, including recent AABB criteria, and sensitivity and specificity of these criteria, as well as of detection by active and passive surveillance, were determined. Twenty of 51,440 platelet units transfused (0.004%; 389/million) were bacterially contaminated by active surveillance and resulted in 5 STR occurring 9-24 h post-transfusion; none of these STR had been reported by passive surveillance. STR occurred only in neutropenic patients transfused with high bacterial loads. A total of 284 transfusion reactions (0.55%) were reported by passive surveillance. None of these patients had received contaminated platelets. However, 6 to 93 (2.1-32.7%) of these 284 reactions met one or more STR criteria, and sensitivity of STR criteria varied from 5.1% to 45.5%. These results document the continued occurrence of bacterial contamination of platelets resulting in STR in neutropenic patients, failure of passive surveillance to detect STR and lack of specificity of STR criteria. These findings highlight the limitations of reported national STR data based on passive surveillance and the need to implement further measures to address this problem such as secondary testing or use of pathogen reduction technologies.
    Blood 11/2015; DOI:10.1182/blood-2015-07-655944
  • H. Liu · X. Sun ·

    Blood 11/2015; 126(21):2436-2436. DOI:10.1182/blood-2015-08-664722

  • Blood 11/2015; 126(21):2349-2351. DOI:10.1182/blood-2015-10-672659

  • Blood 11/2015; 126(21):2376-2382. DOI:10.1182/blood-2015-05-640979
  • H. Sun ·

    Blood 11/2015; 126(21):2352-2353. DOI:10.1182/blood-2015-09-669077

  • Blood 11/2015; 126(21):2370-2375. DOI:10.1182/blood-2015-06-641043

  • Blood 11/2015; 126(21):2351-2352. DOI:10.1182/blood-2015-10-671370
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    ABSTRACT: Enhanced expression of ecotropic viral integration site-1 (EVI-1) occurs in approximately 10% of acute myeloid leukemia (AML) patients and is associated with a very poor disease outcome. Patients with EVI-1 positive AML have poor initial responses to chemotherapy and high relapse rates, indicating an urgent need for alternative treatment strategies improving clinical outcome for these patients. Since treatment of acute pro-myelocytic (APL) patients with all trans retinoid acid (ATRA) has improved the survival of these patients substantially, we investigated whether ATRA might also be effective for the subgroup of AML patients with EVI-1 overexpression. Here, we show that a substantial part of the EVI-1 positive AML cases respond to ATRA by induction of differentiation and decreased clonogenic capacity of myeloid blasts. Most importantly, we demonstrate that in vivo treatment of primary EVI-1 positive AML with ATRA leads to a significant reduction in leukemic engraftment. Altogether, our results show that a considerable part of the EVI-1 positive primary AML cases are sensitive to ATRA, suggesting that combining ATRA with the currently used conventional chemotherapy might be a promising treatment strategy decreasing relapse rates and enhancing complete remissions in this poor prognostic subgroup of AML patients.
    Blood 11/2015; DOI:10.1182/blood-2015-07-653840
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    ABSTRACT: Many patients with hematologic malignancies cannot tolerate hematopoietic cell transplantation (HCT), while others may not have a compatible human leukocyte antigen matched donor. To overcome these limitations we optimized a conditioning regimen employing anti-CD45 radioimmunotherapy (RIT) replacing total body irradiation (TBI) prior to haploidentical HCT in a murine model. Mice received 200-400 μCi (90)Y-anti-CD45 antibody (Ab; 30F11), with or without fludarabine (FLU; 5 days starting day -8), with cyclophosphamide (CY; days -2 and +2) for graft-versus-host disease prophylaxis, and 1.5 × 10(7) haploidentical donor bone marrow cells (day 0). Haploidentical bone marrow transplantation (BMT) with 300 μCi (90)Y-anti-CD45 RIT and CY, without TBI or FLU, led to mixed chimeras with 81.3 ± 10.6% mean donor origin CD8(+) cells detected one month after BMT, and remained stable (85.5 ± 11% mean donor origin CD8(+) cells) 6 months after haploidentical BMT. High chimerism levels were induced across multiple hematopoietic lineages 28 days after haploidentical BMT with 69.3 ± 14.1%, 75.6 ± 20.2%, and 88.5 ± 11.8% CD3(+) T cells, B220(+) B cells, and CD11b(+) myeloid cells, respectively. Fifty percent of SJL leukemia-bearing mice treated with 400 μCi (90)Y-DOTA-30F11, CY, and haploidentical BMT were cured and lived >200 days. Mice treated with 200 μCi (90)Y-DOTA-30F11 had a median overall survival (OS) of 73 days, while untreated leukemic mice had a median OS of 34 days (p<0.001, Mantel-Cox test). RIT-mediated haploidentical BMT without TBI may increase treatment options for aggressive hematologic malignancies.
    Blood 11/2015; DOI:10.1182/blood-2014-12-617019
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    ABSTRACT: Deep remission and prolonged disease-free survival can be achieved with first-line chemoimmunotherapy (CIT), such as combined fludarabine, cyclophosphamide, and rituximab, in the majority of patients with chronic lymphocytic leukemia (CLL). More modest results are reported with less intense regimens like obinutuzumab plus chlorambucil. Clinical assessment has limited sensitivity in detecting residual disease responsible for subsequent relapse, even including morphologic bone marrow (BM) evaluation. Multi-color flow cytometry and polymerase-chain reaction (PCR)-based methods can detect minimal residual disease (MRD) to a sensitivity of at least 1:10,000 (10(-4)). Achieving BM MRD-negative complete remission (CR) is associated with superior progression-free and overall survival; MRD status is the single best post-treatment predictor of long-term outcomes after CIT. Newer oral B cell receptor signaling pathway inhibitors are highly effective at controlling disease, but best monotherapy responses are typically partial remission, and patients must remain on treatment to maintain disease control. Therapeutic progress is still needed for CLL. We propose that targeting MRD provides opportunity to realize this progress. Achieving BM MRD-negative CR is a pre-requisite for long-term unmaintained disease-free survival and potential for cure. We review available methodologies for detecting MRD and correlations with post-treatment outcomes. We discuss the potential utility of MRD to direct individualized therapy. Finally, we discuss the importance of MRD-negative status as a surrogate marker for longer PFS in clinical studies to allow more rapid determination of clinical benefit.
    Blood 11/2015; DOI:10.1182/blood-2015-08-634816