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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]
  • Limited-stage DLBCL: its patient selection
    • Authors: Persky; D. O.
      Pages: 155 - 156
      Keywords: Free Research Articles
      PubDate: 2018-01-11T09:00:32-08:00
      DOI: 10.1182/blood-2017-11-813915
      Issue No: Vol. 131, No. 2 (2018)
       
  • Choosing ibrutinib wisely
    • Authors: Awan; F. T.
      Pages: 156 - 157
      Keywords: Free Research Articles
      PubDate: 2018-01-11T09:00:32-08:00
      DOI: 10.1182/blood-2017-11-813907
      Issue No: Vol. 131, No. 2 (2018)
       
  • NOTCHing down a win for megakaryocytes
    • Authors: Taoudi; S.
      Pages: 158 - 159
      Keywords: Free Research Articles
      PubDate: 2018-01-11T09:00:32-08:00
      DOI: 10.1182/blood-2017-11-815464
      Issue No: Vol. 131, No. 2 (2018)
       
  • Clinicogenetic risk modeling in ATL
    • Authors: Yoshida, N; Weinstock, D. M.
      Pages: 159 - 160
      Keywords: Free Research Articles
      PubDate: 2018-01-11T09:00:32-08:00
      DOI: 10.1182/blood-2017-11-815472
      Issue No: Vol. 131, No. 2 (2018)
       
  • NK cell destiny after haploSCT with PT-Cy
    • Authors: Peled, A; Nagler, A.
      Pages: 161 - 162
      Keywords: Free Research Articles
      PubDate: 2018-01-11T09:00:32-08:00
      DOI: 10.1182/blood-2017-10-811117
      Issue No: Vol. 131, No. 2 (2018)
       
  • How I manage monoclonal gammopathy of undetermined significance
    • Authors: Go, R. S; Rajkumar, S. V.
      Pages: 163 - 173
      Abstract: Monoclonal gammopathy of undetermined significance (MGUS) is, in many ways, a unique hematologic entity. Unlike most hematologic conditions in which the diagnosis is intentional and credited to hematologists, the discovery of MGUS is most often incidental and made by nonhematologists. MGUS is considered an obligate precursor to several lymphoplasmacytic malignancies, including immunoglobulin light-chain amyloidosis, multiple myeloma, and Waldenström macroglobulinemia. Therefore, long-term follow-up is generally recommended. Despite its high prevalence, there is surprisingly limited evidence to inform best clinical practice both at the time of diagnosis and during follow-up. We present 7 vignettes to illustrate common clinical management questions that arise during the course of MGUS. Where evidence is present, we provide a concise summary of the literature and clear recommendations on management. Where evidence is lacking, we describe how we practice and provide a rationale for our approach. We also discuss the potential harms associated with MGUS diagnosis, a topic that is rarely, if ever, broached between patients and providers, or even considered in academic debate.
      Keywords: Multiple Myeloma, How I Treat, Free Research Articles, Lymphoid Neoplasia, Clinical Trials and Observations
      PubDate: 2018-01-11T09:00:32-08:00
      DOI: 10.1182/blood-2017-09-807560
      Issue No: Vol. 131, No. 2 (2018)
       
  • R-CHOP 14 with or without radiotherapy in nonbulky limited-stage diffuse
           large B-cell lymphoma
    • Authors: Lamy, T; Damaj, G, Soubeyran, P, Gyan, E, Cartron, G, Bouabdallah, K, Gressin, R, Cornillon, J, Banos, A, Le Du, K, Benchalal, M, Moles, M.-P, Le Gouill, S, Fleury, J, Godmer, P, Maisonneuve, H, Deconinck, E, Houot, R, Laribi, K, Marolleau, J. P, Tournilhac, O, Branger, B, Devillers, A, Vuillez, J. P, Fest, T, Colombat, P, Costes, V, Szablewski, V, Bene, M. C, Delwail, V, on behalf of the LYSA Group
      Pages: 174 - 181
      Abstract: The benefit of radiotherapy (RT) after chemotherapy in limited-stage diffuse large B-cell lymphoma (DLBCL) remains controversial. We conducted a randomized trial in patients with nonbulky limited-stage DLBCL to evaluate the benefit of RT after rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP). Patients were stratified according to the modified International Prognostic Index, including lactate dehydrogenase, Eastern Cooperative Oncology Group performance status, age, and disease stage. The patients received 4 or 6 consecutive cycles of R-CHOP delivered once every 2 weeks, followed or not by RT at 40 Gy delivered 4 weeks after the last R-CHOP cycle. All patients were evaluated by fluorodeoxyglucose-positron emission tomography scans performed at baseline, after 4 cycles of R-CHOP, and at the end of treatment. The primary objective of the trial was event-free survival (EFS) from randomization. The trial randomly assigned 165 patients in the R-CHOP arm and 169 in the R-CHOP plus RT arm. In an intent-to-treat analysis with a median follow-up of 64 months, 5-year EFS was not statistically significantly different between the 2 arms, with 89% ± 2.9% in the R-CHOP arm vs 92% ± 2.4% in the R-CHOP plus RT arm (hazard ratio, 0.61; 95% confidence interval [CI], 0.3-1.2; P = .18). Overall survival was also not different at 92% (95% CI, 89.5%-94.5%) for patients assigned to R-CHOP alone and 96% (95% CI, 94.3%-97.7%) for those assigned to R-CHOP plus RT (P = not significant). R-CHOP alone is not inferior to R-CHOP followed by RT in patients with nonbulky limited-stage DLBCL. This trial was registered at www.clinicaltrials.gov as #NCT00841945.
      Keywords: Free Research Articles, Lymphoid Neoplasia, Clinical Trials and Observations
      PubDate: 2018-01-11T09:00:32-08:00
      DOI: 10.1182/blood-2017-07-793984
      Issue No: Vol. 131, No. 2 (2018)
       
  • Single-agent ibrutinib in relapsed or refractory follicular lymphoma: a
           phase 2 consortium trial
    • Authors: Bartlett, N. L; Costello, B. A, LaPlant, B. R, Ansell, S. M, Kuruvilla, J. G, Reeder, C. B, Thye, L. S, Anderson, D. M, Krysiak, K, Ramirez, C, Qi, J, Siegel, B. A, Griffith, M, Griffith, O. L, Gomez, F, Fehniger, T. A.
      Pages: 182 - 190
      Abstract: Most patients with follicular lymphoma (FL) experience multiple relapses necessitating subsequent lines of therapy. Ibrutinib, a Bruton tyrosine kinase (BTK) inhibitor approved for the treatment of several B-cell malignancies, showed promising activity in FL in a phase 1 study. We report the results of a phase 2 trial evaluating ibrutinib in recurrent FL. Forty patients with recurrent FL were treated with ibrutinib 560 mg/d until progression or intolerance. The primary end point was overall response rate (ORR). Exploratory analyses included correlations of outcome with recurrent mutations identified in a cancer gene panel that used next-generation sequencing in pretreatment biopsies from 31 patients and results of early interim positron emission tomography/computed tomography scans in 20 patients. ORR was 37.5% with a complete response rate of 12.5%, median progression-free survival (PFS) of 14 months, and 2-year PFS of 20.4%. Response rates were significantly higher among patients whose disease was sensitive to rituximab (52.6%) compared with those who were rituximab refractory (16.7%) (P = .04). CARD11 mutations were present in 16% of patients (5 of 31) and predicted resistance to ibrutinib with only wild-type patients responding (P = .002). Maximum standardized uptake value at cycle 1 day 8 correlated with response and PFS. Ibrutinib was well-tolerated with a toxicity profile similar to labeled indications. Ibrutinib is a well-tolerated treatment with modest activity in relapsed FL. Evaluation of BTK inhibitors in earlier lines of therapy may be warranted on the basis of improved response rates in rituximab-sensitive disease. Somatic mutations such as CARD11 may have an impact on response to ibrutinib, may inform clinical decisions, and should be evaluated in larger data sets. This trial was registered at www.clinicaltrials.gov as #NCT01849263.
      Keywords: Free Research Articles, Lymphoid Neoplasia, Clinical Trials and Observations
      PubDate: 2018-01-11T09:00:32-08:00
      DOI: 10.1182/blood-2017-09-804641
      Issue No: Vol. 131, No. 2 (2018)
       
  • Human NOTCH4 is a key target of RUNX1 in megakaryocytic differentiation
    • Authors: Li, Y; Jin, C, Bai, H, Gao, Y, Sun, S, Chen, L, Qin, L, Liu, P. P, Cheng, L, Wang, Q.-F.
      Pages: 191 - 201
      Abstract: Megakaryocytes (MKs) in adult marrow produce platelets that play important roles in blood coagulation and hemostasis. Monoallelic mutations of the master transcription factor gene RUNX1 lead to familial platelet disorder (FPD) characterized by defective MK and platelet development. However, the molecular mechanisms of FPD remain unclear. Previously, we generated human induced pluripotent stem cells (iPSCs) from patients with FPD containing a RUNX1 nonsense mutation. Production of MKs from the FPD-iPSCs was reduced, and targeted correction of the RUNX1 mutation restored MK production. In this study, we used isogenic pairs of FPD-iPSCs and the MK differentiation system to identify RUNX1 target genes. Using integrative genomic analysis of hematopoietic progenitor cells generated from FPD-iPSCs, and mutation-corrected isogenic controls, we identified 2 gene sets the transcription of which is either up- or downregulated by RUNX1 in mutation-corrected iPSCs. Notably, NOTCH4 expression was negatively controlled by RUNX1 via a novel regulatory DNA element within the locus, and we examined its involvement in MK generation. Specific inactivation of NOTCH4 by an improved CRISPR-Cas9 system in human iPSCs enhanced megakaryopoiesis. Moreover, small molecules known to inhibit Notch signaling promoted MK generation from both normal human iPSCs and postnatal CD34+ hematopoietic stem and progenitor cells. Our study newly identified NOTCH4 as a RUNX1 target gene and revealed a previously unappreciated role of NOTCH4 signaling in promoting human megakaryopoiesis. Our work suggests that human iPSCs with monogenic mutations have the potential to serve as an invaluable resource for discovery of novel druggable targets.
      Keywords: Hematopoiesis and Stem Cells, Platelets and Thrombopoiesis
      PubDate: 2018-01-11T09:00:32-08:00
      DOI: 10.1182/blood-2017-04-780379
      Issue No: Vol. 131, No. 2 (2018)
       
  • Decitabine enhances targeting of AML cells by CD34+ progenitor-derived NK
           cells in NOD/SCID/IL2Rgnull mice
    • Authors: Cany, J; Roeven, M. W. H, Hoogstad-van Evert, J. S, Hobo, W, Maas, F, Franco Fernandez, R, Blijlevens, N. M. A, van der Velden, W. J, Huls, G, Jansen, J. H, Schaap, N. P. M, Dolstra, H.
      Pages: 202 - 214
      Abstract: Combining natural killer (NK) cell adoptive transfer with hypomethylating agents (HMAs) is an attractive therapeutic approach for patients with acute myeloid leukemia (AML). However, data regarding the impact of HMAs on NK cell functionality are mostly derived from in vitro studies with high nonclinical relevant drug concentrations. In the present study, we report a comparative study of azacitidine (AZA) and decitabine (DAC) in combination with allogeneic NK cells generated from CD34+ hematopoietic stem and progenitor cells (HSPC-NK cells) in in vitro and in vivo AML models. In vitro, low-dose HMAs did not impair viability of HSPC-NK cells. Furthermore, low-dose DAC preserved HSPC-NK killing, proliferation, and interferon gamma production capacity, whereas AZA diminished their proliferation and reactivity. Importantly, we showed HMAs and HSPC-NK cells could potently work together to target AML cell lines and patient AML blasts. In vivo, both agents exerted a significant delay in AML progression in NOD/SCID/IL2Rgnull mice, but the persistence of adoptively transferred HSPC-NK cells was not affected. Infused NK cells showed sustained expression of most activating receptors, upregulated NKp44 expression, and remarkable killer cell immunoglobulin-like receptor acquisition. Most importantly, only DAC potentiated HSPC-NK cell anti-leukemic activity in vivo. Besides upregulation of NKG2D- and DNAM-1–activating ligands on AML cells, DAC enhanced messenger RNA expression of inflammatory cytokines, perforin, and TRAIL by HSPC-NK cells. In addition, treatment resulted in increased numbers of HSPC-NK cells in the bone marrow compartment, suggesting that DAC could positively modulate NK cell activity, trafficking, and tumor targeting. These data provide a rationale to explore combination therapy of adoptive HSPC-NK cells and DAC in patients with AML.
      Keywords: Immunobiology and Immunotherapy, Transplantation, Myeloid Neoplasia
      PubDate: 2018-01-11T09:00:32-08:00
      DOI: 10.1182/blood-2017-06-790204
      Issue No: Vol. 131, No. 2 (2018)
       
  • Prognostic relevance of integrated genetic profiling in adult T-cell
           leukemia/lymphoma
    • Authors: Kataoka, K; Iwanaga, M, Yasunaga, J.-i, Nagata, Y, Kitanaka, A, Kameda, T, Yoshimitsu, M, Shiraishi, Y, Sato-Otsubo, A, Sanada, M, Chiba, K, Tanaka, H, Ochi, Y, Aoki, K, Suzuki, H, Shiozawa, Y, Yoshizato, T, Sato, Y, Yoshida, K, Nosaka, K, Hishizawa, M, Itonaga, H, Imaizumi, Y, Munakata, W, Shide, K, Kubuki, Y, Hidaka, T, Nakamaki, T, Ishiyama, K, Miyawaki, S, Ishii, R, Nureki, O, Tobinai, K, Miyazaki, Y, Takaori-Kondo, A, Shibata, T, Miyano, S, Ishitsuka, K, Utsunomiya, A, Shimoda, K, Matsuoka, M, Watanabe, T, Ogawa, S.
      Pages: 215 - 225
      Abstract: Adult T-cell leukemia/lymphoma (ATL) is a heterogeneous group of peripheral T-cell malignancies characterized by human T-cell leukemia virus type-1 infection, whose genetic profile has recently been fully investigated. However, it is still poorly understood how these alterations affect clinical features and prognosis. We investigated the effects of genetic alterations commonly found in ATL on disease phenotypes and clinical outcomes, based on genotyping data obtained from 414 and 463 ATL patients using targeted-capture sequencing and single nucleotide polymorphism array karyotyping, respectively. Aggressive (acute/lymphoma) subtypes were associated with an increased burden of genetic and epigenetic alterations, higher frequencies of TP53 and IRF4 mutations, and many copy number alterations (CNAs), including PD-L1 amplifications and CDKN2A deletions, compared with indolent (chronic/smoldering) subtypes. By contrast, STAT3 mutations were more characteristic of indolent ATL. Higher numbers of somatic mutations and CNAs significantly correlated with worse survival. In a multivariate analysis incorporating both clinical factors and genetic alterations, the Japan Clinical Oncology Group prognostic index high-risk, older age, PRKCB mutations, and PD-L1 amplifications were independent poor prognostic factors in aggressive ATL. In indolent ATL, IRF4 mutations, PD-L1 amplifications, and CDKN2A deletions were significantly associated with shorter survival, although the chronic subtype with unfavorable clinical factors was only marginally significant. Thus, somatic alterations characterizing aggressive diseases predict worse prognosis in indolent ATL, among which PD-L1 amplifications are a strong genetic predictor in both aggressive and indolent ATL. ATL subtypes are further classified into molecularly distinct subsets with different prognosis. Genetic profiling might contribute to improved prognostication and management of ATL patients.
      Keywords: Lymphoid Neoplasia, Clinical Trials and Observations
      PubDate: 2018-01-11T09:00:32-08:00
      DOI: 10.1182/blood-2017-01-761874
      Issue No: Vol. 131, No. 2 (2018)
       
  • FOXP1 expression is a prognostic biomarker in follicular lymphoma treated
           with rituximab and chemotherapy
    • Authors: Mottok, A; Jurinovic, V, Farinha, P, Rosenwald, A, Leich, E, Ott, G, Horn, H, Klapper, W, Boesl, M, Hiddemann, W, Steidl, C, Connors, J. M, Sehn, L. H, Gascoyne, R. D, Hoster, E, Weigert, O, Kridel, R.
      Pages: 226 - 235
      Abstract: Follicular lymphoma (FL) is a clinically and molecularly highly heterogeneous disease, yet prognostication relies predominantly on clinical tools. We recently demonstrated that integration of mutation status of 7 genes, including EZH2 and MEF2B, improves risk stratification. We mined gene expression data to uncover genes that are differentially expressed in EZH2- and MEF2B-mutated cases. We focused on FOXP1 and assessed its protein expression by immunohistochemistry (IHC) in 763 tissue biopsies. For outcome correlation, a population-based training cohort of 142 patients with FL treated with rituximab, cyclophosphamide, vincristine, and prednisone, and a clinical trial validation cohort comprising 395 patients treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) ± rituximab were used. We found FOXP1 to be significantly downregulated in both EZH2- and MEF2B-mutated cases. By IHC, 76 specimens in the training cohort (54%) had high FOXP1 expression (>10%), which was associated with reduced 5-year failure-free survival (FFS) rates (55% vs 70%). In the validation cohort, high FOXP1 expression status was observed in 248 patients (63%) and correlated with significantly shorter FFS in patients treated with R-CHOP (hazard ratio [HR], 1.95; P = .017) but not in patients treated with CHOP (HR, 1.15; P = .44). The impact of high FOXP1 expression on FFS in immunochemotherapy-treated patients was additional to the Follicular Lymphoma International Prognostic Index. High FOXP1 expression was associated with distinct molecular features such as TP53 mutations, expression of IRF4, and gene expression signatures reminiscent of dark zone germinal center or activated B cells. In summary, FOXP1 is a downstream phenotypic commonality of gene mutations and predicts outcome following rituximab-containing regimens.
      Keywords: Lymphoid Neoplasia
      PubDate: 2018-01-11T09:00:32-08:00
      DOI: 10.1182/blood-2017-08-799080
      Issue No: Vol. 131, No. 2 (2018)
       
  • Inhibition of heme oxygenase ameliorates anemia and reduces iron overload
           in a {beta}-thalassemia mouse model
    • Authors: Garcia-Santos, D; Hamdi, A, Saxova, Z, Fillebeen, C, Pantopoulos, K, Horvathova, M, Ponka, P.
      Pages: 236 - 246
      Abstract: Thalassemias are a heterogeneous group of red blood cell disorders, considered a major cause of morbidity and mortality among genetic diseases. However, there is still no universally available cure for thalassemias. The underlying basis of thalassemia pathology is the premature apoptotic destruction of erythroblasts causing ineffective erythropoiesis. In β-thalassemia, β-globin synthesis is reduced causing α-globin accumulation. Unpaired globin chains, with heme attached to them, accumulate in thalassemic erythroblasts causing oxidative stress and the premature cell death. We hypothesize that in β-thalassemia heme oxygenase (HO) 1 could play a pathogenic role in the development of anemia and ineffective erythropoiesis. To test this hypothesis, we exploited a mouse model of β-thalassemia intermedia, Th3/+. We observed that HO inhibition using tin protoporphyrin IX (SnPP) decreased heme-iron recycling in the liver and ameliorated anemia in the Th3/+ mice. SnPP administration led to a decrease in erythropoietin and increase in hepcidin serum levels, changes that were accompanied by an alleviation of ineffective erythropoiesis in Th3/+ mice. Additionally, the bone marrow from Th3/+ mice treated with SnPP exhibited decreased heme catabolism and diminished iron release as well as reduced apoptosis. Our results indicate that the iron released from heme because of HO activity contributes to the pathophysiology of thalassemia. Therefore, new therapies that suppress heme catabolism may be beneficial in ameliorating the anemia and ineffective erythropoiesis in thalassemias.
      Keywords: Red Cells, Iron, and Erythropoiesis
      PubDate: 2018-01-11T09:00:32-08:00
      DOI: 10.1182/blood-2017-07-798728
      Issue No: Vol. 131, No. 2 (2018)
       
  • NK cell recovery after haploidentical HSCT with posttransplant
           cyclophosphamide: dynamics and clinical implications
    • Authors: Russo, A; Oliveira, G, Berglund, S, Greco, R, Gambacorta, V, Cieri, N, Toffalori, C, Zito, L, Lorentino, F, Piemontese, S, Morelli, M, Giglio, F, Assanelli, A, Stanghellini, M. T. L, Bonini, C, Peccatori, J, Ciceri, F, Luznik, L, Vago, L.
      Pages: 247 - 262
      Abstract: The use of posttransplant cyclophosphamide (PT-Cy) as graft-versus-host disease (GVHD) prophylaxis has revolutionized haploidentical hematopoietic stem cell transplantation (HSCT), allowing safe infusion of unmanipulated T cell–replete grafts. PT-Cy selectively eliminates proliferating alloreactive T cells, but whether and how it affects natural killer (NK) cells and their alloreactivity is largely unknown. Here we characterized NK cell dynamics in 17 patients who received unmanipulated haploidentical grafts, containing high numbers of mature NK cells, according to PT-Cy–based protocols in 2 independent centers. In both series, we documented robust proliferation of donor-derived NK cells immediately after HSCT. After infusion of Cy, a marked reduction of proliferating NK cells was evident, suggesting selective purging of dividing cells. Supporting this hypothesis, proliferating NK cells did not express aldehyde dehydrogenase and were killed by Cy in vitro. After ablation of mature NK cells, starting from day 15 after HSCT and favored by the high levels of interleukin-15 present in patients' sera, immature NK cells (CD62L+NKG2A+KIR–) became highly prevalent, possibly directly stemming from infused hematopoietic stem cells. Importantly, also putatively alloreactive single KIR+ NK cells were eliminated by PT-Cy and were thus decreased in numbers and antileukemic potential at day 30 after HSCT. As a consequence, in an extended series of 99 haplo-HSCT with PT-Cy, we found no significant difference in progression-free survival between patients with or without predicted NK alloreactivity (42% vs 52% at 1 year, P = NS). Our data suggest that the majority of mature NK cells infused with unmanipulated grafts are lost upon PT-Cy administration, blunting NK cell alloreactivity in this transplantation setting.
      Keywords: Immunobiology and Immunotherapy, Transplantation
      PubDate: 2018-01-11T09:00:32-08:00
      DOI: 10.1182/blood-2017-05-780668
      Issue No: Vol. 131, No. 2 (2018)
       
  • Efficacy and safety of ruxolitinib in regularly transfused patients with
           thalassemia: results from a phase 2a study
    • Authors: Taher, A. T; Karakas, Z, Cassinerio, E, Siritanaratkul, N, Kattamis, A, Maggio, A, Rivella, S, Hollaender, N, Mahuzier, B, Gadbaw, B, Aydinok, Y.
      Pages: 263 - 265
      Keywords: Transfusion Medicine, Red Cells, Iron, and Erythropoiesis, Clinical Trials and Observations
      PubDate: 2018-01-11T09:00:32-08:00
      DOI: 10.1182/blood-2017-06-790121
      Issue No: Vol. 131, No. 2 (2018)
       
  • Histiocytic sarcoma: a population-based analysis of incidence, demographic
           disparities, and long-term outcomes
    • Authors: Kommalapati, A; Tella, S. H, Durkin, M, Go, R. S, Goyal, G.
      Pages: 265 - 268
      Keywords: Myeloid Neoplasia, Lymphoid Neoplasia, Clinical Trials and Observations
      PubDate: 2018-01-11T09:00:32-08:00
      DOI: 10.1182/blood-2017-10-812495
      Issue No: Vol. 131, No. 2 (2018)
       
  • Talaromyces marneffei and dysplastic neutrophils on blood smear in newly
           diagnosed HIV
    • Authors: Othman, J; Brown, C. M.
      Pages: 269 - 269
      Keywords: Free Research Articles, BloodWork, Phagocytes, Granulocytes, and Myelopoiesis
      PubDate: 2018-01-11T09:00:32-08:00
      DOI: 10.1182/blood-2017-10-809285
      Issue No: Vol. 131, No. 2 (2018)
       
  • When a marginal zone-type lymphocytosis mimics large granular lymphocytes
    • Authors: Derrieux, C; Klein, E.
      Pages: 270 - 270
      Keywords: Free Research Articles, BloodWork, Lymphoid Neoplasia
      PubDate: 2018-01-11T09:00:32-08:00
      DOI: 10.1182/blood-2017-09-807933
      Issue No: Vol. 131, No. 2 (2018)
       
 
 
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