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Journal Cover
Blood
Journal Prestige (SJR): 6.434
Citation Impact (citeScore): 7
Number of Followers: 306  
 
  Full-text available via subscription Subscription journal
ISSN (Print) 0006-4971 - ISSN (Online) 1528-0020
Published by American Society of Hematology Homepage  [2 journals]
  • Introduction to a review series on advances in multiple myeloma
    • Authors: Avet-Loiseau H.
      Pages: 621 - 621
      Keywords: Lymphoid Neoplasia, Review Series
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-11-877795
      Issue No: Vol. 133, No. 7 (2019)
       
  • Megakaryocytes from fat: a new recipe for platelets
    • Authors: Balduini A.
      Pages: 623 - 625
      Keywords: Free Research Articles
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-12-889766
      Issue No: Vol. 133, No. 7 (2019)
       
  • IDH2 inhibition: another piece to the puzzle
    • Authors: Bullinger L.
      Pages: 625 - 626
      Keywords: Free Research Articles
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-12-891481
      Issue No: Vol. 133, No. 7 (2019)
       
  • Off-target effects of carfilzomib that cause cardiotoxicity
    • Authors: Moreb J. S.
      Pages: 626 - 628
      Keywords: Free Research Articles
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-12-889758
      Issue No: Vol. 133, No. 7 (2019)
       
  • Yet another susceptibility variant for ALL: whats next'
    • Authors: Schmiegelow K.
      Pages: 628 - 629
      Keywords: Free Research Articles
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-12-891564
      Issue No: Vol. 133, No. 7 (2019)
       
  • More than one pathway: novel treatment for ITP
    • Authors: Neunert, C. E; Lambert, M. P.
      Pages: 629 - 630
      Keywords: Free Research Articles
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-12-892778
      Issue No: Vol. 133, No. 7 (2019)
       
  • Hepatocyte tPA: where have you been hiding'
    • Authors: Gonias S. L.
      Pages: 631 - 632
      Keywords: Free Research Articles
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-12-891515
      Issue No: Vol. 133, No. 7 (2019)
       
  • Megakaryocytes and platelets from a novel human adipose tissue-derived
           mesenchymal stem cell line
    • Authors: Tozawa, K; Ono-Uruga, Y, Yazawa, M, Mori, T, Murata, M, Okamoto, S, Ikeda, Y, Matsubara, Y.
      Pages: 633 - 643
      Abstract: The clinical need for platelet transfusions is increasing; however, donor-dependent platelet transfusions are associated with practical problems, such as the limited supply and the risk of infection. Thus, we developed a manufacturing system for platelets from a donor-independent cell source: a human adipose-derived mesenchymal stromal/stem cell line (ASCL). The ASCL was obtained using an upside-down culture flask method and satisfied the minimal criteria for defining mesenchymal stem cells (MSCs) by The International Society for Cellular Therapy. The ASCL showed its proliferation capacity for ≥2 months without any abnormal karyotypes. The ASCL was cultured in megakaryocyte induction media. ASCL-derived megakaryocytes were obtained, with a peak at day 8 of culture, and ASCL-derived platelets (ASCL-PLTs) were obtained, with a peak at day 12 of culture. We observed that CD42b+ cells expressed an MSC marker (CD90) which is related to cell adhesion. Compared with peripheral platelets, ASCL-PLTs exhibit higher levels of PAC1 binding, P-selectin surface exposure, ristocetin-induced platelet aggregation, and ADP-induced platelet aggregation, as well as similar levels of fibrinogen binding and collagen-induced platelet aggregation. ASCL-PLTs have lower epinephrine-induced platelet aggregation. The pattern of in vivo kinetics after infusion into irradiated immunodeficient NOD.Cg-PrkdcscidIl2rgtm1Wjl/SzJ mice was similar to that of platelet concentrates. ASCL-PLTs have similar characteristics to those of peripheral platelets and might have an additional function as MSCs. The establishment of the ASCL and its differentiation into ASCL-PLTs do not require gene transfer, and endogenous thrombopoietin is used for differentiation. The present protocol is a simple method that does not require feeder cells, further enhancing the clinical application of our approach.
      Keywords: Thrombocytopenia, Transfusion Medicine, Plenary Papers, Free Research Articles, Platelets and Thrombopoiesis
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-04-842641
      Issue No: Vol. 133, No. 7 (2019)
       
  • Imaging in multiple myeloma: How' When'
    • Authors: Zamagni, E; Tacchetti, P, Cavo, M.
      Pages: 644 - 651
      Abstract: Bone disease is the most frequent feature of multiple myeloma (MM) and represents a marker of end-organ damage; it is used to establish the diagnosis and to dictate the immediate need for therapy. For this reason, imaging plays a significant role in the management of MM patients. Although conventional radiography has traditionally been the standard imaging modality, its low sensitivity in detecting osteolytic lesions and inability to evaluate response to therapy has called for the use of more sophisticated techniques, such as whole-body low-dose computed tomography (WBLDCT), whole-body magnetic resonance imaging, and 18F-fluorodeoxyglucose–positron emission tomography/computed tomography (PET/CT). In this review, the advantages, indications of use, and applications of the 3 techniques in the management of patients with MM in different settings will be discussed. The European Myeloma Network and the European Society for Medical Oncology guidelines have recommended WBLDCT as the imaging modality of choice for the initial assessment of MM-related lytic bone lesions. Magnetic resonance imaging is the gold-standard imaging modality for detection of bone marrow involvement, whereas PET/CT provides valuable prognostic data and is the preferred technique for assessment of response to therapy. Standardization of most of the techniques is ongoing.
      Keywords: Multiple Myeloma, Lymphoid Neoplasia, Review Articles, Review Series, Clinical Trials and Observations
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-08-825356
      Issue No: Vol. 133, No. 7 (2019)
       
  • Pros and cons of frontline autologous transplant in multiple myeloma: the
           debate over timing
    • Authors: Kumar, S. K; Buadi, F. K, Rajkumar, S. V.
      Pages: 652 - 659
      Abstract: The treatment landscape for multiple myeloma has dramatically changed over the past decade with the introduction of several new classes of drugs, which are very effective at controlling the disease for prolonged periods of time, especially when used in multidrug combinations. Prior to the advent of these new agents, peripheral blood autologous stem cell transplantation (ASCT) was the mainstay of therapy for patients who were eligible to undergo the procedure, with deep and durable responses in the majority of patients. Despite the introduction of more effective therapies, ASCT continues to play an important role in overall management of younger patients, where it has been integrated with the other therapeutic approaches to provide maximum benefit. Recent phase 3 trials have once again confirmed the survival benefit associated with ASCT in myeloma. Retrospective studies have also demonstrated the feasibility of using ASCT at the time of first relapse rather than as a component of the initial treatment. Significant geographical variations exist in the use of ASCT, especially between the United States and Europe in terms of its use as part of upfront therapy. Much of these differences are driven by the availability of drugs and drug combinations for initial therapy of myeloma as well as maintenance approaches post-ASCT. It is amply clear from these trials that ASCT will continue to play an important role in management of myeloma and is likely to be used as a platform for enhancing the efficacy of other treatment modalities that are currently in development.
      Keywords: Multiple Myeloma, Lymphoid Neoplasia, Review Articles, Review Series, Clinical Trials and Observations
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-08-825349
      Issue No: Vol. 133, No. 7 (2019)
       
  • Toward personalized treatment in multiple myeloma based on molecular
           characteristics
    • Authors: Pawlyn, C; Davies, F. E.
      Pages: 660 - 675
      Abstract: To date, the choice of therapy for an individual multiple myeloma patient has been based on clinical factors such as age and comorbidities. The widespread evolution, validation, and clinical utilization of molecular technologies, such as fluorescence in situ hybridization and next-generation sequencing has enabled the identification of a number of prognostic and predictive biomarkers for progression-free survival, overall survival, and treatment response. In this review, we argue that in order to continue to improve myeloma patient outcomes incorporating such biomarkers into the routine diagnostic workup of patients will allow for the use of personalized, biologically based treatments.
      Keywords: Multiple Myeloma, Lymphoid Neoplasia, Review Articles, Review Series, Clinical Trials and Observations
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-09-825331
      Issue No: Vol. 133, No. 7 (2019)
       
  • Molecular remission and response patterns in patients with mutant-IDH2
           acute myeloid leukemia treated with enasidenib
    • Authors: Stein, E. M; DiNardo, C. D, Fathi, A. T, Pollyea, D. A, Stone, R. M, Altman, J. K, Roboz, G. J, Patel, M. R, Collins, R, Flinn, I. W, Sekeres, M. A, Stein, A. S, Kantarjian, H. M, Levine, R. L, Vyas, P, MacBeth, K. J, Tosolini, A, VanOostendorp, J, Xu, Q, Gupta, I, Lila, T, Risueno, A, Yen, K. E, Wu, B, Attar, E. C, Tallman, M. S, de Botton, S.
      Pages: 676 - 687
      Abstract: Approximately 8% to 19% of patients with acute myeloid leukemia (AML) have isocitrate dehydrogenase-2 (IDH2) mutations, which occur at active site arginine residues R140 and R172. IDH2 mutations produce an oncometabolite, 2-hydroxyglutarate (2-HG), which leads to DNA and histone hypermethylation and impaired hematopoietic differentiation. Enasidenib is an oral inhibitor of mutant-IDH2 proteins. This first-in-human phase 1/2 study evaluated enasidenib doses of 50 to 650 mg/d, administered in continuous 28-day cycles, in patients with mutant-IDH2 hematologic malignancies. Overall, 214 of 345 patients (62%) with relapsed or refractory (R/R) AML received enasidenib, 100 mg/d. Median age was 68 years. Forty-two patients (19.6%) attained complete remission (CR), 19 patients (10.3%) proceeded to an allogeneic bone marrow transplant, and the overall response rate was 38.8% (95% confidence interval [CI], 32.2-45.7). Median overall survival was 8.8 months (95% CI, 7.7-9.6). Response and survival were comparable among patients with IDH2-R140 or IDH2-R172 mutations. Response rates were similar among patients who, at study entry, were in relapse (37.7%) or were refractory to intensive (37.5%) or nonintensive (43.2%) therapies. Sixty-six (43.1%) red blood cell transfusion–dependent and 53 (40.2%) platelet transfusion–dependent patients achieved transfusion independence. The magnitude of 2-HG reduction on study was associated with CR in IDH2-R172 patients. Clearance of mutant-IDH2 clones was also associated with achievement of CR. Among all 345 patients, the most common grade 3 or 4 treatment-related adverse events were hyperbilirubinemia (10%), thrombocytopenia (7%), and IDH differentiation syndrome (6%). Enasidenib was well tolerated and induced molecular remissions and hematologic responses in patients with AML for whom prior treatments had failed. The study is registered at www.clinicaltrials.gov as #NCT01915498.
      Keywords: Myeloid Neoplasia, Clinical Trials and Observations
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-08-869008
      Issue No: Vol. 133, No. 7 (2019)
       
  • Serial transplantation reveals a critical role for endoglin in
           hematopoietic stem cell quiescence
    • Authors: Borges, L; Oliveira, V. K. P, Baik, J, Bendall, S. C, Perlingeiro, R. C. R.
      Pages: 688 - 696
      Abstract: Transforming growth factor β (TGF-β) is well known for its important function in hematopoietic stem cell (HSC) quiescence. However, the molecular mechanism underlining this function remains obscure. Endoglin (Eng), a type III receptor for the TGF-β superfamily, has been shown to selectively mark long-term HSCs; however, its necessity in adult HSCs is unknown due to embryonic lethality. Using conditional deletion of Eng combined with serial transplantation, we show that this TGF-β receptor is critical to maintain the HSC pool. Transplantation of Eng-deleted whole bone marrow or purified HSCs into lethally irradiated mice results in a profound engraftment defect in tertiary and quaternary recipients. Cell cycle analysis of primary grafts revealed decreased frequency of HSCs in G0, suggesting that lack of Eng impairs reentry of HSCs to quiescence. Using cytometry by time of flight (CyTOF) to evaluate the activity of signaling pathways in individual HSCs, we find that Eng is required within the Lin–Sca+Kit+–CD48– CD150+ fraction for canonical and noncanonical TGF-β signaling, as indicated by decreased phosphorylation of SMAD2/3 and the p38 MAPK-activated protein kinase 2, respectively. These findings support an essential role for Eng in positively modulating TGF-β signaling to ensure maintenance of HSC quiescence.
      Keywords: Hematopoiesis and Stem Cells
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-09-874677
      Issue No: Vol. 133, No. 7 (2019)
       
  • GM-CSF inhibition reduces cytokine release syndrome and neuroinflammation
           but enhances CAR-T cell function in xenografts
    • Authors: Sterner, R. M; Sakemura, R, Cox, M. J, Yang, N, Khadka, R. H, Forsman, C. L, Hansen, M. J, Jin, F, Ayasoufi, K, Hefazi, M, Schick, K. J, Walters, D. K, Ahmed, O, Chappell, D, Sahmoud, T, Durrant, C, Nevala, W. K, Patnaik, M. M, Pease, L. R, Hedin, K. E, Kay, N. E, Johnson, A. J, Kenderian, S. S.
      Pages: 697 - 709
      Abstract: Chimeric antigen receptor T (CAR-T) cell therapy is a new pillar in cancer therapeutics; however, its application is limited by the associated toxicities. These include cytokine release syndrome (CRS) and neurotoxicity. Although the IL-6R antagonist tocilizumab is approved for treatment of CRS, there is no approved treatment of neurotoxicity associated with CD19-targeted CAR-T (CART19) cell therapy. Recent data suggest that monocytes and macrophages contribute to the development of CRS and neurotoxicity after CAR-T cell therapy. Therefore, we investigated neutralizing granulocyte-macrophage colony-stimulating factor (GM-CSF) as a potential strategy to manage CART19 cell–associated toxicities. In this study, we show that GM-CSF neutralization with lenzilumab does not inhibit CART19 cell function in vitro or in vivo. Moreover, CART19 cell proliferation was enhanced and durable control of leukemic disease was maintained better in patient-derived xenografts after GM-CSF neutralization with lenzilumab. In a patient acute lymphoblastic leukemia xenograft model of CRS and neuroinflammation (NI), GM-CSF neutralization resulted in a reduction of myeloid and T cell infiltration in the central nervous system and a significant reduction in NI and prevention of CRS. Finally, we generated GM-CSF–deficient CART19 cells through CRISPR/Cas9 disruption of GM-CSF during CAR-T cell manufacturing. These GM-CSFk/o CAR-T cells maintained normal functions and had enhanced antitumor activity in vivo, as well as improved overall survival, compared with CART19 cells. Together, these studies illuminate a novel approach to abrogate NI and CRS through GM-CSF neutralization, which may potentially enhance CAR-T cell function. Phase 2 studies with lenzilumab in combination with CART19 cell therapy are planned.
      Keywords: Immunobiology and Immunotherapy, Gene Therapy
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-10-881722
      Issue No: Vol. 133, No. 7 (2019)
       
  • Molecular mechanisms of carfilzomib-induced cardiotoxicity in mice and the
           emerging cardioprotective role of metformin
    • Authors: Efentakis, P; Kremastiotis, G, Varela, A, Nikolaou, P.-E, Papanagnou, E.-D, Davos, C. H, Tsoumani, M, Agrogiannis, G, Konstantinidou, A, Kastritis, E, Kanaki, Z, Iliodromitis, E. K, Klinakis, A, Dimopoulos, M. A, Trougakos, I. P, Andreadou, I, Terpos, E.
      Pages: 710 - 723
      Abstract: Carfilzomib (Cfz), an irreversible proteasome inhibitor licensed for relapsed/refractory myeloma, is associated with cardiotoxicity in humans. We sought to establish the optimal protocol of Cfz-induced cardiac dysfunction, to investigate the underlying molecular-signaling and, based on the findings, to evaluate the cardioprotective potency of metformin (Met). Mice were randomized into protocols 1 and 2 (control and Cfz for 1 and 2 consecutive days, respectively); protocols 3 and 4 (control and alternate doses of Cfz for 6 and 14 days, respectively); protocols 5A and 5B (control and Cfz, intermittent doses on days 0, 1 [5A] and 0, 1, 7, and 8 [5B] for 13 days); protocols 6A and 6B (pharmacological intervention; control, Cfz, Cfz+Met and Met for 2 and 6 days, respectively); and protocol 7 (bortezomib). Cfz was administered at 8 mg/kg (IP) and Met at 140 mg/kg (per os). Cfz resulted in significant reduction of proteasomal activity in heart and peripheral blood mononuclear cells in all protocols except protocols 5A and 5B. Echocardiography demonstrated that Cfz led to a significant fractional shortening (FS) depression in protocols 2 and 3, a borderline dysfunction in protocols 1 and 4, and had no detrimental effect on protocols 5A and 5B. Molecular analysis revealed that Cfz inhibited AMPKα/mTORC1 pathways derived from increased PP2A activity in protocol 2, whereas it additionally inhibited phosphatidylinositol 3-kinase/Akt/endothelial nitric oxide synthase pathway in protocol 3. Coadministration of Met prevented Cfz-induced FS reduction and restored AMPKα phosphorylation and autophagic signaling. Conclusively, Cfz decreased left ventricular function through increased PP2A activity and inhibition of AMPKα and its downstream autophagic targets, whereas Met represents a novel promising intervention against Cfz-induced cardiotoxicity.
      Keywords: Multiple Myeloma, Lymphoid Neoplasia
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-06-858415
      Issue No: Vol. 133, No. 7 (2019)
       
  • Novel susceptibility variants at the ERG locus for childhood acute
           lymphoblastic leukemia in Hispanics
    • Authors: Qian, M; Xu, H, Perez-Andreu, V, Roberts, K. G, Zhang, H, Yang, W, Zhang, S, Zhao, X, Smith, C, Devidas, M, Gastier-Foster, J. M, Raetz, E, Larsen, E, Burchard, E. G, Winick, N, Bowman, W. P, Martin, P. L, Borowitz, M, Wood, B, Antillon-Klussmann, F, Pui, C.-H, Mullighan, C. G, Evans, W. E, Hunger, S. P, Relling, M. V, Loh, M. L, Yang, J. J.
      Pages: 724 - 729
      Abstract: Acute lymphoblastic leukemia (ALL) is the most common malignancy in children. Characterized by high levels of Native American ancestry, Hispanics are disproportionally affected by this cancer with high incidence and inferior survival. However, the genetic basis for this disparity remains poorly understood because of a paucity of genome-wide investigation of ALL in Hispanics. Performing a genome-wide association study (GWAS) in 940 Hispanic children with ALL and 681 ancestry-matched non-ALL controls, we identified a novel susceptibility locus in the ERG gene (rs2836365; P = 3.76 x 10–8; odds ratio [OR] = 1.56), with independent validation (P = .01; OR = 1.43). Imputation analyses pointed to a single causal variant driving the association signal at this locus overlapping with putative regulatory DNA elements. The effect size of the ERG risk variant rose with increasing Native American genetic ancestry. The ERG risk genotype was underrepresented in ALL with the ETV6-RUNX1 fusion (P < .0005) but enriched in the TCF3-PBX1 subtype (P < .05). Interestingly, ALL cases with germline ERG risk alleles were significantly less likely to have somatic ERG deletion (P < .05). Our results provide novel insights into genetic predisposition to ALL and its contribution to racial disparity in this cancer.
      Keywords: Pediatric Hematology, Lymphoid Neoplasia, Brief Reports
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-07-862946
      Issue No: Vol. 133, No. 7 (2019)
       
  • Low-dose chidamide restores immune tolerance in ITP in mice and humans
    • Authors: Zhao, H.-y; Ma, Y.-h, Li, D.-q, Sun, T, Li, L.-z, Li, P, Liu, X.-g, Zhou, H, Hou, Y, Liu, Y, Han, P.-p, Zhao, Y.-j, Jing, F.-m, Peng, J, Hou, M.
      Pages: 730 - 742
      Abstract: Increased macrophage phagocytosis of antibody-coated platelets, as well as decreased numbers and/or impaired function of CD4+CD25+Foxp3+ regulatory T (Treg) cells, has been shown to participate in the pathogenesis of immune thrombocytopenia (ITP). Low-dose histone deacetylase inhibitors (HDACi’s) are anti-inflammatory and immunomodulatory agents that can enhance immunosuppression in graft-versus-host disease by increasing the number and function of Foxp3+ Treg cells, but it is unclear whether they have the potential to promote immune tolerance and platelet release in ITP. In this study, we performed in vitro and in vivo experiments and found that a low-dose HDACi (chidamide) alleviated thrombocytopenia in passive and active murine models of ITP. Further, low-dose HDACi’s attenuated macrophage phagocytosis of antibody-coated platelets, stimulated the production of natural Foxp3+ Treg cells, promoted the peripheral conversion of T cells into Treg cells, and restored Treg cell suppression in vivo and in vitro. Finally, we confirmed that low-dose HDACi’s could regulate CTLA4 expression in peripheral blood mononuclear cells through modulation of histone H3K27 acetylation. Low-dose HDACi treatment in ITP could be offset by blocking the effect of CTLA4. Therefore, we propose that low-dose chidamide administration has potential as a novel treatment for ITP in the clinic.
      Keywords: Thrombocytopenia, Platelets and Thrombopoiesis
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-05-847624
      Issue No: Vol. 133, No. 7 (2019)
       
  • An ATF6-tPA pathway in hepatocytes contributes to systemic fibrinolysis
           and is repressed by DACH1
    • Authors: Zheng, Z; Nayak, L, Wang, W, Yurdagul, A, Wang, X, Cai, B, Lapping, S, Ozcan, L, Ramakrishnan, R, Pestell, R. G, Jain, M. K, Tabas, I.
      Pages: 743 - 753
      Abstract: Tissue-type plasminogen activator (tPA) is a major mediator of fibrinolysis and, thereby, prevents excessive coagulation without compromising hemostasis. Studies on tPA regulation have focused on its acute local release by vascular cells in response to injury or other stimuli. However, very little is known about sources, regulation, and fibrinolytic function of noninjury-induced systemic plasma tPA. We explore the role and regulation of hepatocyte-derived tPA as a source of basal plasma tPA activity and as a contributor to fibrinolysis after vascular injury. We show that hepatocyte tPA is downregulated by a pathway in which the corepressor DACH1 represses ATF6, which is an inducer of the tPA gene Plat. Hepatocyte-DACH1–knockout mice show increases in liver Plat, circulating tPA, fibrinolytic activity, bleeding time, and time to thrombosis, which are reversed by silencing hepatocyte Plat. Conversely, hepatocyte-ATF6–knockout mice show decreases in these parameters. The inverse correlation between DACH1 and ATF6/PLAT is conserved in human liver. These findings reveal a regulated pathway in hepatocytes that contributes to basal circulating levels of tPA and to fibrinolysis after vascular injury.
      Keywords: Thrombosis and Hemostasis
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-07-864843
      Issue No: Vol. 133, No. 7 (2019)
       
  • The Hematopoietic Cell Transplant Comorbidity Index predicts survival
           after allogeneic transplant for nonmalignant diseases
    • Authors: Thakar, M. S; Broglie, L, Logan, B, Artz, A, Bunin, N, Burroughs, L. M, Fretham, C, Jacobsohn, D. A, Loren, A. W, Kurtzberg, J, Martinez, C. A, Mineishi, S, Nelson, A. S, Woolfrey, A, Pasquini, M. C, Sorror, M. L.
      Pages: 754 - 762
      Abstract: Despite improvements, mortality after allogeneic hematopoietic cell transplantation (HCT) for nonmalignant diseases remains a significant problem. We evaluated whether pre-HCT conditions defined by the HCT Comorbidity Index (HCT-CI) predict probability of posttransplant survival. Using the Center for International Blood and Marrow Transplant Research database, we identified 4083 patients with nonmalignant diseases transplanted between 2007 and 2014. Primary outcome was overall survival (OS) using the Kaplan-Meier method. Hazard ratios (HRs) were estimated by multivariable Cox regression models. Increasing HCT-CI scores translated to decreased 2-year OS of 82.7%, 80.3%, 74%, and 55.8% for patients with HCT-CI scores of 0, 1 to 2, 3 to 4, and ≥5, respectively, regardless of conditioning intensity. HCT-CI scores of 1 to 2 did not differ relative to scores of 0 (HR, 1.12 [95% CI, 0.93-1.34]), but HCT-CI of 3 to 4 and ≥5 posed significantly greater risks of mortality (HR, 1.33 [95% CI, 1.09-1.63]; and HR, 2.31 [95% CI, 1.79-2.96], respectively). The effect of HCT-CI differed by disease indication. Patients with acquired aplastic anemia, primary immune deficiencies, and congenital bone marrow failure syndromes with scores ≥3 had increased risk of death after HCT. However, higher HCT-CI scores among hemoglobinopathy patients did not increase mortality risk. In conclusion, this is the largest study to date reporting on patients with nonmalignant diseases demonstrating HCT-CI scores ≥3 that had inferior survival after HCT, except for patients with hemoglobinopathies. Our findings suggest that using the HCT-CI score, in addition to disease-specific factors, could be useful when developing treatment plans for nonmalignant diseases.
      Keywords: Transplantation, Clinical Trials and Observations
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-09-876284
      Issue No: Vol. 133, No. 7 (2019)
       
  • Staging systems use for risk stratification of systemic amyloidosis in the
           era of high-sensitivity troponin T assay
    • Authors: Muchtar, E; Kumar, S. K, Gertz, M. A, Grogan, M, AbouEzzeddine, O. F, Jaffe, A. S, Dispenzieri, A.
      Pages: 763 - 766
      Keywords: Multiple Myeloma, Lymphoid Neoplasia, Clinical Trials and Observations
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-10-875252
      Issue No: Vol. 133, No. 7 (2019)
       
  • Intraocular toxoplasmosis mimicking vitreous lymphoma
    • Authors: Su, R. J; Said, J.
      Pages: 767 - 767
      Keywords: Free Research Articles, BloodWork, Lymphoid Neoplasia
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2018-10-883124
      Issue No: Vol. 133, No. 7 (2019)
       
  • Porpaczy E, Tripolt S, Hoelbl-Kovacic A, et al. Aggressive B-cell
           lymphomas in patients with myelofibrosis receiving JAK1/2 inhibitor
           therapy. Blood. 2018;132(7):694-706.
    • Pages: 768 - 768
      Keywords: Free Research Articles
      PubDate: 2019-02-14T09:00:30-08:00
      DOI: 10.1182/blood-2019-01-895136
      Issue No: Vol. 133, No. 7 (2019)
       
 
 
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