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Journal Cover Blood
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   ISSN (Print) 0006-4971 - ISSN (Online) 1528-0020
   Published by American Society of Hematology Homepage  [1 journal]
  • Introduction to a review series on Hodgkin lymphoma: change is here
    • Authors: Sehn L. H.
      Pages: 1629 - 1630
      Keywords: Free Research Articles, Lymphoid Neoplasia, Review Series, Clinical Trials and Observations
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2018-02-824045
      Issue No: Vol. 131, No. 15 (2018)
       
  • Metabolic strugGLS after FLT3 inhibition in AML
    • Authors: Taylor, S. J; Steidl, U.
      Pages: 1631 - 1632
      Keywords: Free Research Articles
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2018-03-836338
      Issue No: Vol. 131, No. 15 (2018)
       
  • Venetoclax after idelalisib: relevant progress for CLL
    • Authors: Bosch, F; Hallek, M.
      Pages: 1632 - 1633
      Keywords: Free Research Articles
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2018-02-826396
      Issue No: Vol. 131, No. 15 (2018)
       
  • Can genetics resolve what Notch does in HSCs'
    • Authors: Maillard, I; Pear, W. S.
      Pages: 1633 - 1635
      Keywords: Free Research Articles
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2018-02-829069
      Issue No: Vol. 131, No. 15 (2018)
       
  • Lymphoma exosomes reprogram the bone marrow
    • Authors: Whiteside T. L.
      Pages: 1635 - 1636
      Keywords: Free Research Articles
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2018-02-830497
      Issue No: Vol. 131, No. 15 (2018)
       
  • Chemokines: a novel chronic GVHD target
    • Authors: Kitko, C; Levine, J. E.
      Pages: 1636 - 1638
      Keywords: Free Research Articles
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2018-02-829101
      Issue No: Vol. 131, No. 15 (2018)
       
  • Glutaminolysis is a metabolic dependency in FLT3ITD acute myeloid leukemia
           unmasked by FLT3 tyrosine kinase inhibition
    • Authors: Gallipoli, P; Giotopoulos, G, Tzelepis, K, Costa, A. S. H, Vohra, S, Medina-Perez, P, Basheer, F, Marando, L, Di Lisio, L, Dias, J. M. L, Yun, H, Sasca, D, Horton, S. J, Vassiliou, G, Frezza, C, Huntly, B. J. P.
      Pages: 1639 - 1653
      Abstract: FLT3 internal tandem duplication (FLT3ITD) mutations are common in acute myeloid leukemia (AML) associated with poor patient prognosis. Although new-generation FLT3 tyrosine kinase inhibitors (TKI) have shown promising results, the outcome of FLT3ITD AML patients remains poor and demands the identification of novel, specific, and validated therapeutic targets for this highly aggressive AML subtype. Utilizing an unbiased genome-wide clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 screen, we identify GLS, the first enzyme in glutamine metabolism, as synthetically lethal with FLT3-TKI treatment. Using complementary metabolomic and gene-expression analysis, we demonstrate that glutamine metabolism, through its ability to support both mitochondrial function and cellular redox metabolism, becomes a metabolic dependency of FLT3ITD AML, specifically unmasked by FLT3-TKI treatment. We extend these findings to AML subtypes driven by other tyrosine kinase (TK) activating mutations and validate the role of GLS as a clinically actionable therapeutic target in both primary AML and in vivo models. Our work highlights the role of metabolic adaptations as a resistance mechanism to several TKI and suggests glutaminolysis as a therapeutically targetable vulnerability when combined with specific TKI in FLT3ITD and other TK activating mutation–driven leukemias.
      Keywords: Plenary Papers, Myeloid Neoplasia
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-12-820035
      Issue No: Vol. 131, No. 15 (2018)
       
  • Biology of classical Hodgkin lymphoma: implications for prognosis and
           novel therapies
    • Authors: Mottok, A; Steidl, C.
      Pages: 1654 - 1665
      Abstract: Hodgkin lymphoma is considered a prime example of treatment success, with cure rates exceeding 80% using modern combined modality therapies. However, especially in adolescents and young adults, treatment-related toxicity and long-term morbidity still represent persistent challenges. Moreover, outcomes in patients with relapsed or refractory disease remain unfavorable in the era of high-dose chemotherapy and stem-cell transplantation. Hence, there is a high demand for novel and innovative alternative treatment approaches. In recent years, many new therapeutic agents have emerged from preclinical and clinical studies that target molecular hallmarks of Hodgkin lymphoma, including the aberrant phenotype of the tumor cells, deregulated oncogenic pathways, and immune escape. The antibody-drug conjugate brentuximab vedotin and immune checkpoint inhibitors have already shown great success in patients with relapsed/refractory disease, leading to US Food and Drug Administration approval and new trials testing these agents in various clinical settings. The expanding knowledge and understanding of Hodgkin lymphoma biology and disease progression, as well as the development of robust tools for biomarker-driven risk stratification and therapeutic decision making, continue to be fundamentally important for the success of these and other novel agents. We anticipate that the availability and clinical implementation of novel molecular assays will be instrumental in an era of rapid shifts in the treatment landscape of this disease. Here, we review the current knowledge of Hodgkin lymphoma pathobiology, highlighting the related development of novel treatment strategies and prognostic models that hold the promise to continually challenge and change the current standard of care in classical Hodgkin lymphoma.
      Keywords: Lymphoid Neoplasia, Review Articles, Review Series
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-09-772632
      Issue No: Vol. 131, No. 15 (2018)
       
  • Balancing risk and benefit in early-stage classical Hodgkin lymphoma
    • Authors: Bröckelmann, P. J; Sasse, S, Engert, A.
      Pages: 1666 - 1678
      Abstract: With defined chemotherapy and radiotherapy (RT) and risk-adapted treatment, early-stage classical Hodgkin lymphoma (HL) has become curable in a majority of patients. Hence, a major current goal is to reduce treatment-related toxicity while maintaining long-term disease control. Patients with early-stage favorable disease (ie, limited stage without risk factors [RFs]) are frequently treated with 2 cycles of doxorubicin, bleomycin, vinblastine, and dacarbazine (2xABVD) followed by 20-Gy involved-field or involved-site RT (IF/ISRT). In patients with early-stage unfavorable disease (ie, limited stage with RFs), 4 cycles of chemotherapy are usually consolidated with 30-Gy IF/ISRT. Compared with 4xABVD, 2 cycles of bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednisone (2xBEACOPPescalated) followed by 2xABVD improved 5-year progression-free survival (PFS), with similar 5-year overall survival. Recently, treatment strategies based on [18F]fluorodeoxyglucose positron emission tomography (PET) response were evaluated. In early-stage unfavorable HL, a majority of patients achieved a negative interim PET after 2xABVD and an excellent outcome after 4xABVD, whereas in those with a positive interim PET, 2xBEACOPPescalated improved 5-year PFS. Furthermore, a PET-guided RT approach was evaluated to decrease long-term toxicity. Although both the RAPID and H10 trials reported poorer disease control without RT, PET-guided omission of RT can constitute a valid therapeutic option in patients with an increased risk of RT-associated toxicity (eg, because of sex, age, or disease localization). Implementation of drugs such as the anti-CD30 antibody-drug conjugate brentuximab vedotin or the anti–programmed death 1 antibodies nivolumab or pembrolizumab might allow further reduction of overall mortality and improve quality of life in affected patients.
      Keywords: Free Research Articles, Lymphoid Neoplasia, Review Articles, Review Series, Clinical Trials and Observations
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-10-772665
      Issue No: Vol. 131, No. 15 (2018)
       
  • Optimizing therapy in advanced-stage Hodgkin lymphoma
    • Authors: Lim, S. H; Johnson, P. W. M.
      Pages: 1679 - 1688
      Abstract: The treatment of Hodgkin lymphoma has evolved continuously since the introduction of extended-field radiotherapy in the 1960s to involved-field and then involved-node radiotherapy, multiagent chemotherapy, combined chemoradiotherapy, risk-adapted and response-adapted modulation, and, most recently, introduction of antibody-drug conjugates and immune checkpoint-blocking antibodies. These changes have translated into progressively increasing cure rates, so that 10-year survival figures now exceed 80%, compared with
      Keywords: Free Research Articles, Lymphoid Neoplasia, Review Articles, Review Series, Clinical Trials and Observations
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-09-772640
      Issue No: Vol. 131, No. 15 (2018)
       
  • Transplant strategies in relapsed/refractory Hodgkin lymphoma
    • Authors: Shah, G. L; Moskowitz, C. H.
      Pages: 1689 - 1697
      Abstract: The majority of patients with Hodgkin lymphoma (HL) are cured with initial therapy. However, high-dose therapy with autologous hematopoietic cell transplant (AHCT) allows for the cure of an additional portion of patients with relapsed or primary refractory disease. Positron emission tomography–negative complete remission before AHCT is critical for long-term disease control. Several salvage options are available with comparable response rates, and the choice can be dependent of comorbidities and logistics. Radiation therapy can also improve the remission rate and is an important therapeutic option for selected patients. Brentuximab vedotin (BV) maintenance after AHCT is beneficial in patients at high risk for relapse, especially those with more than 1 risk factor, but can have the possibility of significant side effects, primarily neuropathy. Newer agents with novel mechanisms of action are under investigation to improve response rates for patients with subsequent relapse, although are not curative alone. BV and the checkpoint inhibitors nivolumab and pembrolizumab are very effective with limited side effects and can bridge patients to curative allogeneic transplants (allo-HCT). Consideration for immune-mediated toxicities, timing of allogeneic hematopoietic cell transplant based on response, and the potential for increased graft-versus-host disease remain important. Overall, prospective investigations continue to improve outcomes and minimize toxicity for relapsed or primary refractory HL patients.
      Keywords: Lymphoid Neoplasia, Review Articles, Review Series
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-09-772673
      Issue No: Vol. 131, No. 15 (2018)
       
  • Management of relapsed/refractory classical Hodgkin lymphoma in
           transplant-ineligible patients
    • Authors: Mehta-Shah, N; Bartlett, N. L.
      Pages: 1698 - 1703
      Abstract: Addition of brentuximab vedotin, a CD30-targeted antibody–drug conjugate, and the programmed death 1 (PD-1) inhibitors nivolumab and pembrolizumab to the armamentarium for transplant-ineligible relapsed/refractory classical Hodgkin lymphoma has resulted in improved outcomes, including the potential for cure in a small minority of patients. For patients who have failed prior transplant or are unsuitable for dose-intense approaches based on age or comorbidities, an individualized approach with sequential use of single agents such as brentuximab vedotin, PD-1 inhibitors, everolimus, lenalidomide, or conventional agents such as gemcitabine or vinorelbine may result in prolonged survival with a minimal or modest effect on quality of life. Participation in clinical trials evaluating new approaches such as combination immune checkpoint inhibition, novel antibody–drug conjugates, or cellular therapies such as Epstein-Barr virus–directed cytotoxic T lymphocytes and chimeric antigen receptor T cells offer additional options for eligible patients.
      Keywords: Transplantation, Free Research Articles, Lymphoid Neoplasia, Review Articles, Review Series, Clinical Trials and Observations
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-09-772681
      Issue No: Vol. 131, No. 15 (2018)
       
  • Venetoclax for patients with chronic lymphocytic leukemia who progressed
           during or after idelalisib therapy
    • Authors: Coutre, S; Choi, M, Furman, R. R, Eradat, H, Heffner, L, Jones, J. A, Chyla, B, Zhou, L, Agarwal, S, Waskiewicz, T, Verdugo, M, Humerickhouse, R. A, Potluri, J, Wierda, W. G, Davids, M. S.
      Pages: 1704 - 1711
      Abstract: B-cell receptor pathway inhibitors (BCRis) have transformed treatment of chronic lymphocytic leukemia (CLL); however, the efficacy of therapies for patients whose disease is refractory to/relapses after (R/R) BCRis is unknown. Venetoclax is a selective, orally bioavailable BCL-2 inhibitor with activity in patients with CLL, including those who are heavily pretreated or have 17p deletion. This phase 2 study prospectively evaluated venetoclax in patients with R/R CLL after ibrutinib or idelalisib; here we report on patients who received idelalisib as the last BCRi before enrollment. Venetoclax was initiated at 20 mg daily, followed by intrapatient ramp-up to 400 mg daily. Primary objectives included efficacy (objective response rate [ORR]) and safety of venetoclax. The study enrolled 36 patients who previously received idelalisib (ORR, 67% [24/36]); 2 patients achieved complete remission, and 1 had complete remission with incomplete bone marrow recovery. Median progression-free survival (PFS) has not yet been reached; estimated 12-month PFS was 79%. The most common adverse events (AEs; all grades) were neutropenia (56%), diarrhea (42%), upper respiratory tract infection (39%), thrombocytopenia (36%), nausea (31%), fatigue (28%), cough (22%), rash (22%), and anemia (22%). Grade 3 or 4 AEs were primarily hematologic (neutropenia [50%], thrombocytopenia [25%], and anemia [17%]). No patients experienced tumor lysis syndrome. Venetoclax demonstrated promising clinical activity and favorable tolerability in patients with CLL whose disease progressed during or after idelalisib therapy. This trial was registered at www.clinicaltrials.gov as #NCT02141282.
      Keywords: Free Research Articles, Lymphoid Neoplasia, Clinical Trials and Observations
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-06-788133
      Issue No: Vol. 131, No. 15 (2018)
       
  • Canonical Notch signaling is dispensable for adult steady-state and stress
           myelo-erythropoiesis
    • Authors: Duarte, S; Woll, P. S, Buza-Vidas, N, Chin, D. W. L, Boukarabila, H, Luis, T. C, Stenson, L, Bouriez-Jones, T, Ferry, H, Mead, A. J, Atkinson, D, Jin, S, Clark, S.-A, Wu, B, Repapi, E, Gray, N, Taylor, S, Mutvei, A. P, Tsoi, Y. L, Nerlov, C, Lendahl, U, Jacobsen, S. E. W.
      Pages: 1712 - 1719
      Abstract: Although an essential role for canonical Notch signaling in generation of hematopoietic stem cells in the embryo and in thymic T-cell development is well established, its role in adult bone marrow (BM) myelopoiesis remains unclear. Some studies, analyzing myeloid progenitors in adult mice with inhibited Notch signaling, implicated distinct roles of canonical Notch signaling in regulation of progenitors for the megakaryocyte, erythroid, and granulocyte-macrophage cell lineages. However, these studies might also have targeted other pathways. Therefore, we specifically deleted, in adult BM, the transcription factor recombination signal-binding protein J (Rbpj), through which canonical signaling from all Notch receptors converges. Notably, detailed progenitor staging established that canonical Notch signaling is fully dispensable for all investigated stages of megakaryocyte, erythroid, and myeloid progenitors in steady state unperturbed hematopoiesis, after competitive BM transplantation, and in stress-induced erythropoiesis. Moreover, expression of key regulators of these hematopoietic lineages and Notch target genes were unaffected by Rbpj deficiency in BM progenitor cells.
      Keywords: Hematopoiesis and Stem Cells
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-06-788505
      Issue No: Vol. 131, No. 15 (2018)
       
  • Extracellular vesicle-mediated transfer of constitutively active
           MyD88L265P engages MyD88wt and activates signaling
    • Authors: Mancek-Keber, M; Lainscek, D, Bencina, M, Chen, J. G, Romih, R, Hunter, Z. R, Treon, S. P, Jerala, R.
      Pages: 1720 - 1729
      Abstract: The link between inflammation and cancer is particularly strong in Waldenström macroglobulinemia (WM), a diffuse large B-cell lymphoma wherein the majority of patients harbor a constitutively active mutation in the innate immune-signaling adaptor myeloid differentiation primary response 88 (MyD88). MyD88Leu265Pro (MyD88L265P) constitutively triggers the myddosome assembly providing a survival signal for cancer cells. Here, we report detection and a functional role of MyD88 in the extracellular vesicles (EVs) shed from WM cells. MyD88L265P was transferred via EVs into the cytoplasm of the recipient mast cells and macrophages, recruiting the endogenous MyD88 that triggered the activation of proinflammatory signaling in the absence of receptor activation. Additionally, internalization of EVs containing MyD88L265P was observed in mice with an effect on the bone marrow microenvironment. MyD88-loaded EVs were detected in the bone marrow aspirates of WM patients thus establishing the physiological role of EVs for MyD88L265P transmission and shaping of the proinflammatory microenvironment. Results establish the mechanism of transmission of signaling complexes via EVs to propagate inflammation as a new mechanism of intercellular communication.
      Keywords: Immunobiology and Immunotherapy
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-09-805499
      Issue No: Vol. 131, No. 15 (2018)
       
  • LSD1 inhibition exerts its antileukemic effect by recommissioning PU.1-
           and C/EBP{alpha}-dependent enhancers in AML
    • Authors: Cusan, M; Cai, S. F, Mohammad, H. P, Krivtsov, A, Chramiec, A, Loizou, E, Witkin, M. D, Smitheman, K. N, Tenen, D. G, Ye, M, Will, B, Steidl, U, Kruger, R. G, Levine, R. L, Rienhoff, H. Y, Koche, R. P, Armstrong, S. A.
      Pages: 1730 - 1742
      Abstract: Epigenetic regulators are recurrently mutated and aberrantly expressed in acute myeloid leukemia (AML). Targeted therapies designed to inhibit these chromatin-modifying enzymes, such as the histone demethylase lysine-specific demethylase 1 (LSD1) and the histone methyltransferase DOT1L, have been developed as novel treatment modalities for these often refractory diseases. A common feature of many of these targeted agents is their ability to induce myeloid differentiation, suggesting that multiple paths toward a myeloid gene expression program can be engaged to relieve the differentiation blockade that is uniformly seen in AML. We performed a comparative assessment of chromatin dynamics during the treatment of mixed lineage leukemia (MLL)-AF9-driven murine leukemias and MLL-rearranged patient-derived xenografts using 2 distinct but effective differentiation-inducing targeted epigenetic therapies, the LSD1 inhibitor GSK-LSD1 and the DOT1L inhibitor EPZ4777. Intriguingly, GSK-LSD1 treatment caused global gains in chromatin accessibility, whereas treatment with EPZ4777 caused global losses in accessibility. We captured PU.1 and C/EBPα motif signatures at LSD1 inhibitor-induced dynamic sites and chromatin immunoprecipitation coupled with high-throughput sequencing revealed co-occupancy of these myeloid transcription factors at these sites. Functionally, we confirmed that diminished expression of PU.1 or genetic deletion of C/EBPα in MLL-AF9 cells generates resistance of these leukemias to LSD1 inhibition. These findings reveal that pharmacologic inhibition of LSD1 represents a unique path to overcome the differentiation block in AML for therapeutic benefit.
      Keywords: Myeloid Neoplasia
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-09-807024
      Issue No: Vol. 131, No. 15 (2018)
       
  • Murine chronic graft-versus-host disease proteome profiling discovers
           CCL15 as a novel biomarker in patients
    • Authors: Du, J; Flynn, R, Paz, K, Ren, H.-G, Ogata, Y, Zhang, Q, Gafken, P. R, Storer, B. E, Roy, N. H, Burkhardt, J. K, Mathews, W, Tolar, J, Lee, S. J, Blazar, B. R, Paczesny, S.
      Pages: 1743 - 1754
      Abstract: Improved diagnostic and treatment methods are needed for chronic graft-versus-host disease (cGVHD), the leading cause of late nonrelapse mortality (NRM) in long-term survivors of allogenic hematopoietic cell transplantation. Validated biomarkers that facilitate disease diagnosis and classification generally are lacking in cGVHD. Here, we conducted whole serum proteomics analysis of a well-established murine multiorgan system cGVHD model. We discovered 4 upregulated proteins during cGVHD that are targetable by genetic ablation or blocking antibodies, including the RAS and JUN kinase activator, CRKL, and CXCL7, CCL8, and CCL9 chemokines. Donor T cells lacking CRK/CRKL prevented the generation of cGVHD, germinal center reactions, and macrophage infiltration seen with wild-type T cells. Whereas antibody blockade of CCL8 or CXCL7 was ineffective in treating cGVHD, CCL9 blockade reversed cGVHD clinical manifestations, histopathological changes, and immunopathological hallmarks. Mechanistically, elevated CCL9 expression was present predominantly in vascular smooth muscle cells and uniquely seen in cGVHD mice. Plasma concentrations of CCL15, the human homolog of mouse CCL9, were elevated in a previously published cohort of 211 cGVHD patients compared with controls and associated with NRM. In a cohort of 792 patients, CCL15 measured at day +100 could not predict cGVHD occurring within the next 3 months with clinically relevant sensitivity/specificity. Our findings demonstrate for the first time the utility of preclinical proteomics screening to identify potential new targets for cGVHD and specifically CCL15 as a diagnosis marker for cGVHD. These data warrant prospective biomarker validation studies.
      Keywords: Transplantation
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-08-800623
      Issue No: Vol. 131, No. 15 (2018)
       
  • The phosphotyrosine phosphatase SHP2 promotes anergy in chronic
           lymphocytic leukemia
    • Authors: Schliffke, S; Buhs, S, Bolz, S, Gerull, H, von Wenserski, L, Riecken, K, Fehse, B, Nollau, P, Binder, M.
      Pages: 1755 - 1758
      Keywords: Lymphoid Neoplasia
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-06-788166
      Issue No: Vol. 131, No. 15 (2018)
       
  • A Ser725Arg mutation in Band 3 abolishes transport function and leads to
           anemia and renal tubular acidosis
    • Authors: Yang, E; Seo-Mayer, P, Lezon-Geyda, K, Badior, K. E, Li, J, Casey, J. R, Reithmeier, R. A. F, Gallagher, P. G.
      Pages: 1759 - 1763
      Keywords: Red Cells, Iron, and Erythropoiesis
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2018-01-827725
      Issue No: Vol. 131, No. 15 (2018)
       
  • ALK+ small cell variant of anaplastic large cell lymphoma with leukemic
           presentation
    • Authors: Jiang, X; Zhou, D.
      Pages: 1764 - 1764
      Keywords: Free Research Articles, BloodWork, Lymphoid Neoplasia
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-11-816074
      Issue No: Vol. 131, No. 15 (2018)
       
  • Monomorphic epitheliotropic intestinal T-cell lymphoma involving the
           central nervous system
    • Authors: Kubota, Y; Kusaba, K.
      Pages: 1765 - 1765
      Keywords: Free Research Articles, BloodWork, Lymphoid Neoplasia
      PubDate: 2018-04-12T09:00:28-07:00
      DOI: 10.1182/blood-2017-11-819136
      Issue No: Vol. 131, No. 15 (2018)
       
 
 
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