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Journal Cover
Blood
Journal Prestige (SJR): 6.434
Citation Impact (citeScore): 7
Number of Followers: 262  
 
  Full-text available via subscription Subscription journal
ISSN (Print) 0006-4971 - ISSN (Online) 1528-0020
Published by American Society of Hematology Homepage  [2 journals]
  • CHIPing out PPM1D-mutant hematopoiesis
    • Authors: Kindler; T.
      Pages: 1087 - 1088
      Keywords: Free Research Articles
      PubDate: 2018-09-13T09:00:19-07:00
      DOI: 10.1182/blood-2018-07-861716
      Issue No: Vol. 132, No. 11 (2018)
       
  • The incomparable platelet: holy alveoli!
    • Authors: Looney; M. R.
      Pages: 1088 - 1089
      Keywords: Free Research Articles
      PubDate: 2018-09-13T09:00:19-07:00
      DOI: 10.1182/blood-2018-06-856351
      Issue No: Vol. 132, No. 11 (2018)
       
  • Platelet metabolism meets thrombosis
    • Authors: Chen, Y; Silverstein, R. L.
      Pages: 1089 - 1091
      Keywords: Free Research Articles
      PubDate: 2018-09-13T09:00:19-07:00
      DOI: 10.1182/blood-2018-08-865600
      Issue No: Vol. 132, No. 11 (2018)
       
  • Rhesus pieces: genotype matching of RBCs
    • Authors: Hendrickson, J. E; Tormey, C. A.
      Pages: 1091 - 1093
      Keywords: Free Research Articles
      PubDate: 2018-09-13T09:00:19-07:00
      DOI: 10.1182/blood-2018-07-865634
      Issue No: Vol. 132, No. 11 (2018)
       
  • PPM1D-truncating mutations confer resistance to chemotherapy and
           sensitivity to PPM1D inhibition in hematopoietic cells
    • Authors: Kahn, J. D; Miller, P. G, Silver, A. J, Sellar, R. S, Bhatt, S, Gibson, C, McConkey, M, Adams, D, Mar, B, Mertins, P, Fereshetian, S, Krug, K, Zhu, H, Letai, A, Carr, S. A, Doench, J, Jaiswal, S, Ebert, B. L.
      Pages: 1095 - 1105
      Abstract: Truncating mutations in the terminal exon of protein phosphatase Mg2+/Mn2+ 1D (PPM1D) have been identified in clonal hematopoiesis and myeloid neoplasms, with a striking enrichment in patients previously exposed to chemotherapy. In this study, we demonstrate that truncating PPM1D mutations confer a chemoresistance phenotype, resulting in the selective expansion of PPM1D-mutant hematopoietic cells in the presence of chemotherapy in vitro and in vivo. Clustered regularly interspaced short palindromic repeats (CRISPR)–CRISPR-associated protein-9 nuclease mutational profiling of PPM1D in the presence of chemotherapy selected for the same exon 6 mutations identified in patient samples. These exon 6 mutations encode for a truncated protein that displays elevated expression and activity due to loss of a C-terminal degradation domain. Global phosphoproteomic profiling revealed altered phosphorylation of target proteins in the presence of the mutation, highlighting multiple pathways including the DNA damage response (DDR). In the presence of chemotherapy, PPM1D-mutant cells have an abrogated DDR resulting in altered cell cycle progression, decreased apoptosis, and reduced mitochondrial priming. We demonstrate that treatment with an allosteric, small molecule inhibitor of PPM1D reverts the phosphoproteomic, DDR, apoptotic, and mitochondrial priming changes observed in PPM1D-mutant cells. Finally, we show that the inhibitor preferentially kills PPM1D-mutant cells, sensitizes the cells to chemotherapy, and reverses the chemoresistance phenotype. These results provide an explanation for the enrichment of truncating PPM1D mutations in the blood of patients exposed to chemotherapy and in therapy-related myeloid neoplasms, and demonstrate that PPM1D can be a targeted in the prevention of clonal expansion of PPM1D-mutant cells and the treatment of PPM1D-mutant disease.
      Keywords: Plenary Papers, Myeloid Neoplasia
      PubDate: 2018-09-13T09:00:19-07:00
      DOI: 10.1182/blood-2018-05-850339
      Issue No: Vol. 132, No. 11 (2018)
       
  • Differentiation-based model of hematopoietic stem cell functions and
           lineage pathways
    • Authors: Höfer, T; Rodewald, H.-R.
      Pages: 1106 - 1113
      Abstract: Advances in genetic labeling and barcoding of hematopoietic stem cells (HSCs) in situ now allow direct measurements of physiological HSC output, both quantitatively and qualitatively. Turning on a heritable label in HSCs and measuring the kinetics of label emergence in downstream compartments reveal rates of differentiation and self-renewal of HSCs and progenitor cells, whereas endogenous HSC barcoding probes physiological precursor-product relationships. Labels have been inserted at different stages of the hematopoietic differentiation hierarchy. Recent genetic and functional evidence suggests a phenotype (Tie2+) for tip HSCs. Fate mapping shows that many tip HSCs regularly feed into downstream stages, with individual cells contributing infrequently. Stem and progenitor cells downstream of tip HSCs serve as a major, nearly self-renewing source of day-to-day hematopoiesis, rendering the blood and immune system HSC-independent for extended periods of time. HSCs realize multilineage output, yet, fates restricted to several lineages or even a single lineage have also been observed. Single HSCs within a clone in the bone marrow that develop from a fetal HSC precursor have been observed to express clone-specific fates. Thus, the new tools probing HSC differentiation in situ are progressing beyond assays for HSC activity based on proliferation measurements and fates of transplanted stem cells, and the data challenge lineage interpretations of single-cell gene expression snapshots. Linking in vivo fate analyses to gene expression and other molecular determinants of cell fate will aid in unraveling the mechanisms of lineage commitment and the architecture of physiological hematopoiesis.
      Keywords: Perspectives, Hematopoiesis and Stem Cells
      PubDate: 2018-09-13T09:00:19-07:00
      DOI: 10.1182/blood-2018-03-791517
      Issue No: Vol. 132, No. 11 (2018)
       
  • How I treat the young patient with multiple myeloma
    • Authors: Gandolfi, S; Prada, C. P, Richardson, P. G.
      Pages: 1114 - 1124
      Abstract: The treatment landscape for multiple myeloma has been transformed by the introduction of novel agents, including immunomodulatory drugs, proteasome inhibitors, and monoclonal antibodies. These have been shown to be more effective and generally better tolerated than conventional chemotherapy, with their introduction into clinical practice leading to improved survival. Furthermore, a better understanding of disease biology, improved diagnostic criteria, and the development of sensitive and specific tools for disease prognostication have contributed to better outcome. Treatment in the younger patient can now be individualized based on host and disease features with enhanced monitoring of response and use of high-sensitivity techniques for evaluating residual disease. The current standard of care has been significantly enhanced by novel agents with a paradigm shift toward optional or delayed autologous stem cell transplant as a reasonable choice in selected patients. Conversely, extended treatment with induction of remission followed by maintenance strategies is now a standard of care, conferring prolonged disease control with more manageable toxicities in both the short and long term, as well as improved quality of life.
      Keywords: Multiple Myeloma, How I Treat, Free Research Articles, Lymphoid Neoplasia, Clinical Trials and Observations
      PubDate: 2018-09-13T09:00:19-07:00
      DOI: 10.1182/blood-2017-05-693606
      Issue No: Vol. 132, No. 11 (2018)
       
  • A phase 1 trial of vadastuximab talirine combined with hypomethylating
           agents in patients with CD33-positive AML
    • Authors: Fathi, A. T; Erba, H. P, Lancet, J. E, Stein, E. M, Ravandi, F, Faderl, S, Walter, R. B, Advani, A. S, DeAngelo, D. J, Kovacsovics, T. J, Jillella, A, Bixby, D, Levy, M. Y, OMeara, M. M, Ho, P. A, Voellinger, J, Stein, A. S.
      Pages: 1125 - 1133
      Abstract: Treatment of acute myeloid leukemia (AML) among the elderly is challenging because of intolerance of intensive therapy and therapy-resistant biology. Hypomethylating agents (HMAs) are commonly used, with suboptimal outcomes. Vadastuximab talirine is a CD33-directed antibody conjugated to pyrrolobenzodiazepine (PBD) dimers. Preclinically, HMAs followed by vadastuximab talirine produced upregulated CD33 expression, increased DNA incorporation by PBD, and enhanced cytotoxicity. A combination cohort in a phase 1 study (NCT01902329) assessed safety, tolerability, and activity of vadastuximab talirine with HMAs. Those eligible had Eastern Cooperative Oncology Group status 0 to 1 and previously untreated CD33-positive AML, and declined intensive therapy. Vadastuximab talirine was administered intravenously at 10 μg/kg on last day of HMA (azacitidine or decitabine) infusion in 4-week cycles. Among 53 patients treated, the median age was 75 years. Patients had adverse (38%) or intermediate (62%) cytogenetic risk. Median treatment duration was 19.3 weeks. No dose-limiting toxicities were reported. The majority of adverse events were a result of myelosuppression, with some causing therapy delays. Thirty- and 60-day mortality rates were 2% and 8%, respectively. The composite remission rate (complete remission [CR] and CR with incomplete blood count recovery) was 70%. Fifty-one percent of remissions were minimal residual disease-negative by flow cytometry. Similarly high remission rates were observed in patients with secondary AML, aged at least 75 years, and with adverse cytogenetic risk. Median relapse-free survival and overall survival were 7.7 and 11.3 months, respectively. Compared with historical data for HMA monotherapy, the combination of vadastuximab talirine with HMAs produced a high remission rate, but was accompanied by increased hematologic toxicity.
      Keywords: Myeloid Neoplasia, Clinical Trials and Observations
      PubDate: 2018-09-13T09:00:19-07:00
      DOI: 10.1182/blood-2018-03-841171
      Issue No: Vol. 132, No. 11 (2018)
       
  • Antitumor activity of CAR-T cells targeting the intracellular oncoprotein
           WT1 can be enhanced by vaccination
    • Authors: Akahori, Y; Wang, L, Yoneyama, M, Seo, N, Okumura, S, Miyahara, Y, Amaishi, Y, Okamoto, S, Mineno, J, Ikeda, H, Maki, T, Fujiwara, H, Akatsuka, Y, Kato, T, Shiku, H.
      Pages: 1134 - 1145
      Abstract: The recent success of chimeric antigen receptor (CAR)-T cell therapy for treatment of hematologic malignancies supports further development of treatments for both liquid and solid tumors. However, expansion of CAR-T cell therapy is limited by the availability of surface antigens specific for the tumor while sparing normal cells. There is a rich diversity of tumor antigens from intracellularly expressed proteins that current and conventional CAR-T cells are unable to target. Furthermore, adoptively transferred T cells often suffer from exhaustion and insufficient expansion, in part, because of the immunosuppressive mechanisms operating in tumor-bearing hosts. Therefore, it is necessary to develop means to further activate and expand those CAR-T cells in vivo. The Wilms tumor 1 (WT1) is an intracellular oncogenic transcription factor that is an attractive target for cancer immunotherapy because of its overexpression in a wide range of leukemias and solid tumors, and a low level of expression in normal adult tissues. In the present study, we developed CAR-T cells consisting of a single chain variable fragment (scFv) specific to the WT1235-243/HLA-A*2402 complex. The therapeutic efficacy of our CAR-T cells was demonstrated in a xenograft model, which was further enhanced by vaccination with dendritic cells (DCs) loaded with the corresponding antigen. This enhanced efficacy was mediated, at least partly, by the expansion and activation of CAR-T cells. CAR-T cells shown in the present study not only demonstrate the potential to expand the range of targets available to CAR-T cells, but also provide a proof of concept that efficacy of CAR-T cells targeting peptide/major histocompatibility complex can be boosted by vaccination.
      Keywords: Immunobiology and Immunotherapy
      PubDate: 2018-09-13T09:00:19-07:00
      DOI: 10.1182/blood-2017-08-802926
      Issue No: Vol. 132, No. 11 (2018)
       
  • Oncogenic activation of the STAT3 pathway drives PD-L1 expression in
           natural killer/T-cell lymphoma
    • Authors: Song, T. L; Nairismägi, M.-L, Laurensia, Y, Lim, J.-Q, Tan, J, Li, Z.-M, Pang, W.-L, Kizhakeyil, A, Wijaya, G.-C, Huang, D.-C, Nagarajan, S, Chia, B. K.-H, Cheah, D, Liu, Y.-H, Zhang, F, Rao, H.-L, Tang, T, Wong, E. K.-Y, Bei, J.-X, Iqbal, J, Grigoropoulos, N.-F, Ng, S.-B, Chng, W.-J, Teh, B.-T, Tan, S.-Y, Verma, N. K, Fan, H, Lim, S.-T, Ong, C.-K.
      Pages: 1146 - 1158
      Abstract: Mature T-cell lymphomas, including peripheral T-cell lymphoma (PTCL) and extranodal NK/T-cell lymphoma (NKTL), represent a heterogeneous group of non-Hodgkin lymphomas with dismal outcomes and limited treatment options. To determine the extent of involvement of the JAK/STAT pathway in this malignancy, we performed targeted capture sequencing of 188 genes in this pathway in 171 PTCL and NKTL cases. A total of 272 nonsynonymous somatic mutations in 101 genes were identified in 73% of the samples, including 258 single-nucleotide variants and 14 insertions or deletions. Recurrent mutations were most frequently located in STAT3 and TP53 (15%), followed by JAK3 and JAK1 (6%) and SOCS1 (4%). A high prevalence of STAT3 mutation (21%) was observed specifically in NKTL. Novel STAT3 mutations (p.D427H, E616G, p.E616K, and p.E696K) were shown to increase STAT3 phosphorylation and transcriptional activity of STAT3 in the absence of cytokine, in which p.E616K induced programmed cell death-ligand 1 (PD-L1) expression by robust binding of activated STAT3 to the PD-L1 gene promoter. Consistent with these findings, PD-L1 was overexpressed in NKTL cell lines harboring hotspot STAT3 mutations, and similar findings were observed by the overexpression of p.E616K and p.E616G in the STAT3 wild-type NKTL cell line. Conversely, STAT3 silencing and inhibition decreased PD-L1 expression in STAT3 mutant NKTL cell lines. In NKTL tumors, STAT3 activation correlated significantly with PD-L1 expression. We demonstrated that STAT3 activation confers high PD-L1 expression, which may promote tumor immune evasion. The combination of PD-1/PD-L1 antibodies and STAT3 inhibitors might be a promising therapeutic approach for NKTL, and possibly PTCL.
      Keywords: Immunobiology and Immunotherapy, Lymphoid Neoplasia
      PubDate: 2018-09-13T09:00:19-07:00
      DOI: 10.1182/blood-2018-01-829424
      Issue No: Vol. 132, No. 11 (2018)
       
  • Disparities in survival by insurance status in follicular lymphoma
    • Authors: Goldstein, J. S; Nastoupil, L. J, Han, X, Jemal, A, Ward, E, Flowers, C. R.
      Pages: 1159 - 1166
      Abstract: Follicular lymphoma (FL) is the second most common non-Hodgkin lymphoma and most common indolent non-Hodgkin lymphoma. Lower socioeconomic status is associated with poor outcomes in FL, suggesting that access to care is an important prognostic factor; however, the association between insurance status and FL survival has not been sufficiently examined. The National Cancer Database, a nationwide cancer registry, was used to evaluate 43 648 patients with FL diagnosed between 2004 and 2014. All analyses were performed on 2 cohorts segmented at age 65 years to account for changes in insurance status with Medicare eligibility. Cox proportional hazard models calculated hazard ratios (HRs) with confidence intervals (CIs) for the association between insurance status and overall survival (OS) controlling for the available sociodemographic and prognostic factors. Kaplan-Meier curves display outcomes by insurance status for patients covered by private insurance, no insurance, Medicaid, or Medicare. When compared with patients younger than age 65 years with private insurance, patients younger than age 65 years with no insurance (HR, 1.96; 95% CI, 1.69-2.28), with Medicaid (HR, 1.82; 95% CI, 1.57-2.12), and with Medicare (HR, 1.96; 95% CI, 1.71-2.24) had significantly worse OS after adjusting for sociodemographic and prognostic factors. Compared with patients age 65 years or older with private insurance, those with Medicare only (HR, 1.28; 95% CI, 1.17-1.4) had significantly worse OS. For adults with FL, expanding access to care through insurance has the potential to improve outcomes.
      Keywords: Lymphoid Neoplasia, Clinical Trials and Observations
      PubDate: 2018-09-13T09:00:19-07:00
      DOI: 10.1182/blood-2018-03-839035
      Issue No: Vol. 132, No. 11 (2018)
       
  • Platelets play an essential role in murine lung development through
           Clec-2/podoplanin interaction
    • Authors: Tsukiji, N; Inoue, O, Morimoto, M, Tatsumi, N, Nagatomo, H, Ueta, K, Shirai, T, Sasaki, T, Otake, S, Tamura, S, Tachibana, T, Okabe, M, Hirashima, M, Ozaki, Y, Suzuki-Inoue, K.
      Pages: 1167 - 1179
      Abstract: Platelets participate in not only thrombosis and hemostasis but also other pathophysiological processes, including tumor metastasis and inflammation. However, the putative role of platelets in the development of solid organs has not yet been described. Here, we report that platelets regulate lung development through the interaction between the platelet-activation receptor, C-type lectin-like receptor-2 (Clec-2; encoded by Clec1b), and its ligand, podoplanin, a membrane protein. Clec-2 deletion in mouse platelets led to lung malformation, which caused respiratory failure and neonatal lethality. In these embryos, α-smooth muscle actin-positive alveolar duct myofibroblasts (adMYFs) were almost absent in the primary alveolar septa, which resulted in loss of alveolar elastic fibers and lung malformation. Our data suggest that the lack of adMYFs is caused by abnormal differentiation of lung mesothelial cells (luMCs), the major progenitor of adMYFs. In the developing lung, podoplanin expression is detected in alveolar epithelial cells (AECs), luMCs, and lymphatic endothelial cells (LECs). LEC-specific podoplanin knockout mice showed neonatal lethality and Clec1b–/–-like lung developmental abnormalities. Notably, these Clec1b–/–-like lung abnormalities were also observed after thrombocytopenia or transforming growth factor-β depletion in fetuses. We propose that the interaction between Clec-2 on platelets and podoplanin on LECs stimulates adMYF differentiation of luMCs through transforming growth factor-β signaling, thus regulating normal lung development.
      Keywords: Platelets and Thrombopoiesis
      PubDate: 2018-09-13T09:00:19-07:00
      DOI: 10.1182/blood-2017-12-823369
      Issue No: Vol. 132, No. 11 (2018)
       
  • AMPK-ACC signaling modulates platelet phospholipids and potentiates
           thrombus formation
    • Authors: Lepropre, S; Kautbally, S, Octave, M, Ginion, A, Onselaer, M.-B, Steinberg, G. R, Kemp, B. E, Hego, A, Wera, O, Brouns, S, Swieringa, F, Giera, M, Darley-Usmar, V. M, Ambroise, J, Guigas, B, Heemskerk, J, Bertrand, L, Oury, C, Beauloye, C, Horman, S.
      Pages: 1180 - 1192
      Abstract: AMP-activated protein kinase (AMPK) α1 is activated in platelets on thrombin or collagen stimulation, and as a consequence, phosphorylates and inhibits acetyl-CoA carboxylase (ACC). Because ACC is crucial for the synthesis of fatty acids, which are essential for platelet activation, we hypothesized that this enzyme plays a central regulatory role in platelet function. To investigate this, we used a double knock-in (DKI) mouse model in which the AMPK phosphorylation sites Ser79 on ACC1 and Ser212 on ACC2 were mutated to prevent AMPK signaling to ACC. Suppression of ACC phosphorylation promoted injury-induced arterial thrombosis in vivo and enhanced thrombus growth ex vivo on collagen-coated surfaces under flow. After collagen stimulation, loss of AMPK-ACC signaling was associated with amplified thromboxane generation and dense granule secretion. ACC DKI platelets had increased arachidonic acid-containing phosphatidylethanolamine plasmalogen lipids. In conclusion, AMPK-ACC signaling is coupled to the control of thrombosis by specifically modulating thromboxane and granule release in response to collagen. It appears to achieve this by increasing platelet phospholipid content required for the generation of arachidonic acid, a key mediator of platelet activation.
      Keywords: Platelets and Thrombopoiesis, Thrombosis and Hemostasis
      PubDate: 2018-09-13T09:00:19-07:00
      DOI: 10.1182/blood-2018-02-831503
      Issue No: Vol. 132, No. 11 (2018)
       
  • A factor VIII-nanobody fusion protein forming an ultrastable complex with
           VWF: effect on clearance and antibody formation
    • Authors: Muczynski, V; Casari, C, Moreau, F, Ayme, G, Kawecki, C, Legendre, P, Proulle, V, Christophe, O. D, Denis, C. V, Lenting, P. J.
      Pages: 1193 - 1197
      Abstract: Von Willebrand factor (VWF) modulates factor VIII (FVIII) clearance and the anti-FVIII immune response. Despite the high affinity that defines the FVIII/VWF interaction, association/dissociation kinetics dictates 2% to 5% FVIII being present as free protein. To avoid free FVIII when studying the FVIII-VWF complex in vivo, we designed a FVIII-nanobody fusion protein, with the nanobody part being directed against VWF. This fusion protein, designated FVIII-KB013bv, had a 25-fold higher affinity compared with B-domainless FVIII (BDD-FVIII) for VWF. In vitro analysis revealed full cofactor activity in 1-stage clotting and chromogenic assays (activity/antigen ratio 1.0 ± 0.3 and 1.1 ± 0.3, respectively). In vivo, FVIII-013bv displayed a twofold increased mean residence time compared with BDD-FVIII (3.0 hours vs 1.6 hours). In a tail clip–bleeding assay performed 24 hours after FVIII infusion, blood loss was significantly reduced in mice receiving FVIII-KB013bv vs BDD-FVIII (15 ± 7 μL vs 194 ± 146 μL; P = .0043). Unexpectedly, when examining anti-FVIII antibody formation in FVIII-deficient mice, the immune-response toward FVIII-KB013bv was significantly reduced compared with BDD-FVIII (1/8 vs 14/16 mice produced anti-FVIII antibodies after treatment with FVIII-KB013bv and BDD-FVIII, respectively). Our data show that a stabilized interaction between FVIII and VWF is associated with a prolonged survival of FVIII and a reduced immune response against FVIII.
      Keywords: Thrombosis and Hemostasis, Brief Reports
      PubDate: 2018-09-13T09:00:19-07:00
      DOI: 10.1182/blood-2018-01-829523
      Issue No: Vol. 132, No. 11 (2018)
       
  • RH genotype matching for transfusion support in sickle cell disease
    • Authors: Chou, S. T; Evans, P, Vege, S, Coleman, S. L, Friedman, D. F, Keller, M, Westhoff, C. M.
      Pages: 1198 - 1207
      Abstract: Rh alloimmunization remains a challenge for patients with sickle cell disease (SCD) despite transfusion of serologic Rh C, E, and K antigen-matched red cells. Inheritance of altered RH alleles contributes to the prevalence of Rh antibodies after blood transfusion in patients with SCD and explains approximately one-third of cases. The remainder seem to be stimulated by altered Rh proteins on African American donor red cells. Matching patients with donors on the basis of RH genotype may mitigate Rh alloimmunization, but the feasibility and resources required are not known. We compared RH allele frequencies between patients with SCD (n = 857) and African American donors (n = 587) and showed that RH allele frequencies are similar. Overall, 29% of RHD and 53% of RHCE alleles are altered in patients and African American donors. We modeled RH genotype matching compared with serologic Rh D, C, and E, along with K antigen matching, and found that approximately twice the number of African American donors would be required for RH genotype vs Rh serologic matching at our institution. We demonstrated that African American donor recruitment is necessary to maintain an adequate supply of C-, E-, and K-negative donor units to avoid depleting the Rh-negative (RhD–) blood supply. Our results suggest that prophylactic RH genetic matching for patients with SCD is feasible with a donor pool comprised primarily of African-Americans and would optimize the use of our existing minority donor inventory. The current cost of RH genotyping all minority donors and management of the data remain limiting factors.
      Keywords: Sickle Cell Disease, Transfusion Medicine, Red Cells, Iron, and Erythropoiesis
      PubDate: 2018-09-13T09:00:19-07:00
      DOI: 10.1182/blood-2018-05-851360
      Issue No: Vol. 132, No. 11 (2018)
       
  • Pericardial effusion in Hodgkin lymphoma: a report from the Childrens
           Oncology Group AHOD0031 protocol
    • Authors: Marks, L. J; McCarten, K. M, Pei, Q, Friedman, D. L, Schwartz, C. L, Kelly, K. M.
      Pages: 1208 - 1211
      Keywords: Pediatric Hematology, Lymphoid Neoplasia, Clinical Trials and Observations
      PubDate: 2018-09-13T09:00:19-07:00
      DOI: 10.1182/blood-2018-02-834465
      Issue No: Vol. 132, No. 11 (2018)
       
  • A novel disease-causing synonymous exonic mutation in GATA2 affecting RNA
           splicing
    • Authors: Wehr, C; Grotius, K, Casadei, S, Bleckmann, D, Bode, S. F. N, Frye, B. C, Seidl, M, Gulsuner, S, King, M.-C, Percival, M.-B, Pritchard, C. C, Walsh, T, Wu, D, Keel, S, Salzer, U.
      Pages: 1211 - 1215
      Keywords: Hematopoiesis and Stem Cells, Myeloid Neoplasia, Red Cells, Iron, and Erythropoiesis
      PubDate: 2018-09-13T09:00:19-07:00
      DOI: 10.1182/blood-2018-03-837336
      Issue No: Vol. 132, No. 11 (2018)
       
  • Hairy cell leukemia in a child'!
    • Authors: Bosma, M; Bartels, M.
      Pages: 1216 - 1216
      Keywords: Free Research Articles, BloodWork, Lymphoid Neoplasia
      PubDate: 2018-09-13T09:00:19-07:00
      DOI: 10.1182/blood-2018-06-857938
      Issue No: Vol. 132, No. 11 (2018)
       
 
 
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