Leukemia and Lymphoma (LEUKEMIA LYMPHOMA)

Publisher: Informa Healthcare

Journal description

Leukemia and Lymphoma is an international journal that brings together clinical and laboratory data on lymphomas, leukemias and allied disorders including myeloma and myelodysplastic syndromes. Leukemia and Lymphoma publishes full-length papers, communications and reviews on clinical and therapeutic practice, laboratory diagnosis, pathology, cytology, ultrastructure, cytogenetics and cellular and molecular immunology; the journal aims at a strong clinical-pathologic correlation. Interesting or unusual case reports of importance are also included. In addition, an update is provided on the basic issues and advances in molecular genetics as applied to this field. The journal will provide an important reference source for physicians and scientists who deal essentially with the clinical and laboratory diagnosis, clinical care and therapy of patients with these disorders.

Current impact factor: 2.89

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.891
2013 Impact Factor 2.605
2012 Impact Factor 2.301
2011 Impact Factor 2.58
2010 Impact Factor 2.492
2009 Impact Factor 2.397
2008 Impact Factor 1.939
2007 Impact Factor 1.512
2006 Impact Factor 1.559
2005 Impact Factor 1.295
2004 Impact Factor 1.147
2003 Impact Factor 1.163
2002 Impact Factor 1.335
2001 Impact Factor 1.257
2000 Impact Factor 1.252
1999 Impact Factor 1.14
1998 Impact Factor 1.099
1997 Impact Factor 1.046
1996 Impact Factor 1.134
1995 Impact Factor 0.79
1994 Impact Factor 0.568
1993 Impact Factor 0.622

Impact factor over time

Impact factor

Additional details

5-year impact 2.62
Cited half-life 5.70
Immediacy index 1.00
Eigenfactor 0.02
Article influence 0.89
Website Leukemia and Lymphoma website
Other titles Leukemia & lymphoma (Online), Leukemia and lymphoma
ISSN 1042-8194
OCLC 50166437
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Informa Healthcare

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • On author's personal website or institution website
    • Publisher copyright and source must be acknowledged
    • Non-commercial
    • Must link to publisher version
    • Publisher's version/PDF cannot be used
    • NIH funded authors may post articles to PubMed Central for release 12 months after publication
    • Wellcome Trust authors may deposit in Europe PMC after 6 months
  • Classification
    ​ yellow

Publications in this journal

  • Aspasia Stamatoullas · Rezine Imene · Sylvain Mareschal · Anne Lis Ménard · Hélène Lanic · Marion David · Sylvie Daliphard · Dominique Penther · Emilie Lemasle · Ophélie Cassuto · Pascal Lenain · Nathalie Contentin · Stéphane Lepretre · Fabrice Jardin · Christian Bastard · Hervé Tilly
    Leukemia and Lymphoma 10/2015; DOI:10.3109/10428194.2015.1101096
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    ABSTRACT: This randomized-controlled trial studied the efficacy of palifermin, administered as a dose during HSCT therapy, as primary prophylaxis on paediatric patients with Acute lymphoblastic leukemia in order to reduce Oral Mucositis. Patients in the palifermin group were randomly assigned to receive Palifermin, 60 μg/kg, intravenously as a single dose 3 days before and 0, +1, and +2 post autologous HSCT infusion. The patients in the control group received only a placebo treatment. OM-related assessments were the WHO oral-toxicity scale and the patient-reported outcomes. There was a statistically significant reduction in the incidence of OM grade 3 and 4 in the palifermin group compared to the control group. There was also a reduction in the degree of severity of OM in the palifermin group (1.65 grade respect to 2.33 in the control group). Palifermin could prevent the recurrence of severe OM and improve the quality of life in patients with ALL.
    Leukemia and Lymphoma 10/2015; DOI:10.3109/10428194.2015.1081192
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    ABSTRACT: A decreasing number of new therapeutic drugs reaching the clinic has led to the publication of regulatory guidelines on human microdosing trials by the European Medicines Agency in 2004 and the U.S. Food and Drug Administration in 2006. Microdosing trials are defined by the administration of 1/100(th) of the therapeutic dose and designed to investigate basic drug properties. This review investigates the current application of phase 0 trials in medical research. Thirty-three studies found in PubMed and EMBASE were systematically reviewed for aim and analytical method. Pharmacokinetic studies have been a major focus of phase 0 trials, but drug distribution, drug-drug interactions, imaging, and pharmacogenomics have also been investigated. Common analytical methods were tandem mass liquid chromatography, accelerator mass spectrometry, and positron emission tomography. New ongoing trials are investigating the pharmacodynamics and chemoresistance of marketed drugs, suggesting that the application of phase 0 trials is still evolving.
    Leukemia and Lymphoma 10/2015; DOI:10.3109/10428194.2015.1101097
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    ABSTRACT: To evaluate the feasibility of selecting a mobilization regimen based on the response to induction therapy, we retrospectively analyzed 179 multiple myeloma patients who underwent stem cell mobilization. In comparison of patients who achieved at least a very good partial response (VGPR) to induction therapy and received granulocyte colony stimulating factor (G-CSF) alone and patients who did not achieve a VGPR and received cyclophosphamide (CY) + G-CSF, treatment-related toxicity was greater and neutrophil engraftment was slower in the CY than the G-CSF group. The rate of requisite mobilization (≥ 2.0 x 10(6)/kg) was similar in both groups. Overall and progression-free survival was not different between patients in the G-CSF group and patients who achieved at least VGPR and received CY + G-CSF. In conclusion, response-adapted selection of a mobilization regimen is appropriate. G-CSF alone should be the preferred treatment for patients who achieved at least a VGPR to induction therapy.
    Leukemia and Lymphoma 10/2015; DOI:10.3109/10428194.2015.1102240
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    ABSTRACT: We evaluated the association of baseline prognostic factors with conditional net survival among survivors of six subtypes non-Hodgkin lymphoma using the SEER program data from 2000-2012. Among 2-year survivors, further prognosis markedly improved in Burkitt's (BL) and diffuse large B-cell lymphoma (DLBCL), and became the same as for follicular lymphoma (5-year net survival ≥85%). Mantle cell lymphoma (MCL) demonstrated the worst prognosis of all studied histologies up to 5 years of survivorship. Age and stage lost prognostic significance in BL within 2 years from diagnosis. Racial disparities in net survival disappeared within 2 years for all subtypes, except in chronic lymphocytic leukemia, where black patients had persistently worse prognosis, and in MCL, where they had unexpectedly better prognosis than other races after 2 years. Many baseline factors may lose their initial prognostic value for lymphoma survivors, which should be considered when counseling patients about their prognosis and long-term surveillance.
    Leukemia and Lymphoma 10/2015; DOI:10.3109/10428194.2015.1102246
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    ABSTRACT: Infectious complications are an important risk factor for early mortality in patients with multiple myeloma. However, data about the impact and severity of infections in these patients in the era of new therapies have not been properly analyzed. We have reviewed the incidence and severity of infections complications and infection-related mortality during induction treatment in patients with newly diagnosed myeloma receiving regimens with new drugs within randomized trials. The results show that infections are still a major cause of morbidity especially among elderly patients receiving immunomodulatory drugs seeing in up to 28% of patients in some trials versus less than 10% among transplant-eligible patients. Overall infection-related mortality ranged from 0% to 7% in transplant-ineligible patients with no infection-related deaths in the majority of the trials including younger patients. Strategies directed to further reduce these complications and a better knowledge of their impact in patients treated outside clinical trials are needed.
    Leukemia and Lymphoma 10/2015; DOI:10.3109/10428194.2015.1088647
  • Pilar de la Puente · Feda Azab · Barbara Muz · Micah Luderer · Jack Arbiser · Abdel Kareem Azab
    Leukemia and Lymphoma 09/2015; DOI:10.3109/10428194.2015.1099645
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    ABSTRACT: The frequency of coexisting JAK2(V617F)/MPL and JAK2(V617F)/JAK2 exon-12 mutations has not been previously investigated in MPNs. Poor survival was reported in primary myelofibrosis with low JAK2(V617F) allelic burden. However, mutational status of JAK2 exon-12 or MPL were not reported in these patients. We developed a cost-effective multiplex high resolution melt assay that screens for mutations in JAK2 gene exons-12 and -14 ((V617F)) and MPL gene exon-10. Coexisting mutations with JAK2(V617F) were detected in 2.9% (6/208; two JAK2 exon-12, and four MPL exon-10) patient specimens with known JAK2(V617F) (allelic-burden range: 0.1-96.8%). Coexisting mutations were detected in specimens with <12% JAK2(V617F) allelic burden. Current WHO guidelines, do not recommend further testing once JAK2(V617F) mutation detected in MPNs. Our findings, however, indicate that quantification of JAK2(V617F) allele burden may be clinically relevant in MPNs, and in those with low allelic burden additional testing for JAK2 exon-12 and MPL exon-10 mutation should be pursued.
    Leukemia and Lymphoma 09/2015; DOI:10.3109/10428194.2015.1091932
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    ABSTRACT: This study investigated the cytotoxic effect of oridonin, a diterpenoid isolated from Rabdosia rubescens, in human diffuse large B cell lymphoma (DLBCL) in vitro and in vivo and the potential molecular mechanisms for oridonin-induced cell apoptosis. Oridonin treatment caused reactive oxygen species (ROS)-mediated oxidative DNA damage response (DDR) and the c-Jun N-terminal kinase(JNK) pathway activation, leaded to an induction of intrinsic apoptosis. ROS abolition blocked oridonin-induced apoptosis and attenuated the expression of phospho-histone H2AX and phospho-JNK, indicating that ROS-mediated DNA damage and JNK pathway activation were involved in oridonin-induced apoptosis. The systemic administration of oridonin suppressed the growth of human DLBCL xenografts without showing significant toxicity. These findings suggest that oridonin may have promising therapeutic application in DLBCL.
    Leukemia and Lymphoma 09/2015; DOI:10.3109/10428194.2015.1061127
  • Leukemia and Lymphoma 09/2015; DOI:10.3109/10428194.2015.1099648
  • Leukemia and Lymphoma 09/2015; DOI:10.3109/10428194.2015.1083098
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    ABSTRACT: Background: Rituximab (RXB) ‐containing chemotherapy forms the backbone of treatment for CD20 positive non‐Hodgkin's lymphomas (NHL). RXB is combined with other agents as induction chemotherapy or as a single‐agent maintenance therapy for indolent NHLs. RXB has been associated with reactivation of chronic hepatitis C virus (HCV) infection – a condition that leads to discontinuation of chemotherapy in 45% of patients who experience it. However, there is no data on the occurrence HCV reactivation according to the different types of RXB treatment strategies administered. We evaluated the effect of various RXB‐containing regimens on HCV viremia. Methods: Medical records of all patients with NHL seen at MD Anderson between 01/2008‐05/2014 were screened. Records of those who were treated with RXB‐containing regimens and had HCV RNA levels available before and after chemotherapy were analyzed. HCV reactivation was defined as an increase of HCV RNA of ≥ log IU/mL over prechemotherapy levels. Acute exacerbation of HCV infection (AcEx) was defined as an increase of alanine aminotransferase (ALT) levels of ≥ 3 times upper normal limit in the absence of liver infiltration of cancer, hepatotoxic drugs, recent transfusion, and coinfections. The groups compared were those who received RXB + chemotherapy (induction), with those who received RXB + chemotherapy followed by RXB maintenance therapy. Categorical variables were compared using χ2 or Fisher's exact test and continuous variables were compared using Wilcoxon rank sum test. Within each group, continuous variables before and after chemotherapy were compared using Wilcoxon signed‐rank test. All P values < 0.05 were considered statistically significant. Results: We analyzed 28 HCV‐infected patients (14 prospectively; 14 retrospectively) who received RXB‐containing chemotherapy. Most patients were males (64%), whites (57%), and had a median age of 54.7 years (interquartile range, 47.8 – 61.4 years). Types of NHL included diffuse large B cell (54%), follicular (21%), marginal zone B cell (11%), mantle cell (4%), lymphoplasmacytic (4%), small lymphocytic (4%), and undetermined low grade B cell (4%) lymphomas; mostly Ann Arbor stage IV (82%). HCV genotype 1 was the most predominant strain (72%). Very few patients (12%) had cirrhosis when RXB chemotherapy was initiated. HCV treatment was administered before RXB chemotherapy in 9 (32%) patients but no one had resolved viremia (sustained virological response) at the time of cancer treatment. Overall, 43 courses of RXB‐containing chemotherapy were administered, mostly as induction therapy (n = 39; 91%). Most common RXBcontaining regimens administered were R‐CHOP (n = 13; 30%), R‐ICE (n = 6; 14%), and RXB with bendamustine (n = 5; 12%). In the entire cohort, when compared to pre‐chemotherapy baseline levels, there were significant elevations in HCV RNA (median, log IU/mL; 6.6 vs. 6.9; P = 0.005) and ALT (median, IU/L; 50 vs. 115; P < 0.0001) only after administration of RXB as induction chemotherapy, with no significant changes being found after RXB maintenance chemotherapy [HCV RNA (6.8 vs. 6.7; P = 1.0); ALT (37 vs. 59; P = 0.07)] (See Figure). When compared to maintenance therapy, those who received induction therapy attained peak HCV RNA (median, days; 590 vs. 140; P = 0.006) and peak ALT (median, days; 172 vs. 43; P = 0.02) earlier after RXB administration. HCV reactivation occurred only when induction chemotherapy was administered (n = 7). Doses of RXB‐containing chemotherapeutic agents had to be modified (reduced or postponed) in 4 out of the 7 (57%) episodes of HCV reactivation. Median relapse‐free survival for those who had dose modifications was lower than those without (14.6 months vs. 20.1 months; P = 0.13). Conclusion: HCV reactivation occurs after administration of RXB as a part of induction, but not maintenance chemotherapy for NHL. This virologic condition is associated with dose modification of RXB‐containing chemotherapeutic regimens in over one‐half of cases.
    Leukemia and Lymphoma 09/2015; DOI:10.3109/10428194.2015.1099649
  • Natalia Sotelo · Daniel Prieto · Noé Seija · Cecilia Abreu · Rosario Duran · Magdalena Gil · Victoria Irigoin · Cecilia Guillermo · Ana Ines Landoni · Raul Gabus · Guillermo Dighiero · Pablo Oppezzo
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    ABSTRACT: Chronic Lymphocytic Leukemia (CLL) is an incurable disease characterized by the accumulation of clonal B lymphocytes with a mature phenotype, resulting from a balance between cell proliferation and apoptotic death. It is widely accepted that a continuous crosstalk between cancer cells and local/distant host environment is required for tumor growth which could favor disease progression and drug resistance. Among of the main actors of this dynamic and reciprocal interplay between tumoral cells and their microenvironment also exists the nano-sized vesicles called exosomes. Emerging evidence indicates that exosomes play a key role in tumor-host crosstalk and their secretion, composition, and functional capacity are altered as tumors progress to an aggressive phenotype. The exosomes released by cancer cells can also signal to stromal cells within the cancer microenvironment, thus impacting tumor cell growth, metastasis, and angiogenesis.In CLL, has been shown that plasma derived MVs mediate AKT activation in bone marrow stromal cells. Moreover, a recent work of Yeh et al. identified a specific exosomal microRNA signature and suggests that highest amount of exosomes in CLL could be related to BCR signaling. Since several works state that exosomes promote tumor progression and that these small vesicles are increased in CLL plasma samples, we wondered: a) Is there a common proteomic profile on exosomes from CLL? b) Which proteins are differentially expressed in exosomes during CLL evolution? and c) how could these proteins affect CLL progression? To this aim we studied 12 CLLs which were segregated into indolent UM and Mut CLLs and progresssive UM CLLs (n=4 for each group). Indolent and progressive patients were characterized by IgVH gene profile, AID and lipoprotein lipase expression. Samples from progressive patients were further segregated from indolent CLLs by clinical parameters, such as a highly progressive disease, rapid lymphocyte doubling time (1 year), lymphocytosis > 50.000/mm3 and FCR treatment indicated before 3 years after debut. PB from progressive CLLs was obtained at debut and before treatment, whereas for indolent patients, PB was taken at debut and after 3-4 years of follow-up. Exosomes were purified from plasma on an iodixanol gradient under a differential centrifugation protocol, and their protein expression profile analyzed by nano liquid chromatography/Mass Spectrometry (LC-MS/MS). Our results show for the first time a common proteomic signature on exosomes from CLL and describe a differential expression pattern between indolent and progressive CLLs. Taking into account that exosomes have a role in oncogenic transformation and cancer progression we focused on the proteins that has been overexpressed in the plasma derived exosomes of those patients whose CLL has a clinical progression. Our data underline three proteins i.e. gamma-catenin, S100-A9 and thioredoxin1 that appears only in the plasma of patients with active CLL progression. Interestingly, these proteins are associated with key signaling pathways as cancer progression, cellular proliferation and tissue inflammation which lead us to speculate about the involvement of these proteins in CLL progression. http://dx.doi.org/10.3109/10428194.2015.1080893
    Leukemia and Lymphoma 09/2015;
  • Pablo Morande · Xiao-Jie Yan · Natalia Sotelo · Daniel Prieto · Noé Seija · Martina Crispo · Nicholas Chiorazzi · Pablo Oppezzo
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    ABSTRACT: Chronic Lymphocytic Leukemia (CLL) shows a highly variable disease course, partly explained by the diverse combinations of somatic mutations whose were recently uncovered by whole-exome sequencing (WES) analysis. In physiological conditions, the enzyme Activation-induced cytidine deaminase (AID) initiates somatic hypermutation (SHM) and class switch recombination (CSR) of the immunoglobulin genes, which are necessary for an effective immune response. As a trade-off for the benefits brought about by its physiological roles, AID can also contribute to cellular transformation and tumor progression by aberrantly mutagenizing genes outside the Ig locus (off-target mutations). We previously described that progressive CLL patients aberrantly express AID in CLL B-cells of PB (Oppezzo et al., Blood 2005), and that its expression is associated with worse patient outcome (Palacios et al., Blood 2010 and Patten, et al., Blood 2012). The aims of the present work were: a) to evaluate the role of AID in CLL clonal evolution, and b) to identify AID signature mutations during disease progression. To these aims we used the transgenic Eu-TCL1 mice, a murine model that mimics a progressive and unmutated CLL disease, and crossed it with a transgenic strain overexpressing AID under the control of the actin promoter. Double transgenic actin-AID/Eu-TCL1 mice (DT) were viable and showed no evident inborn alterations. Presence at the DNA genomic level of AID and TCL1 genes and gene expression at RNA levels was verified by quantitative PCR in PB and spleen cells, for both transgenes. DT mice expressed TCL1 and showed higher expression of AID as compared to its TCL1 counterpart, for both PB and spleen cells (n=5, p<0.05). To compare the aggressiveness of CLL disease in the DT strain with that of the Eu-TCL1 model, we chose two time points: 6 months of age as a pre-leukemic stage of the Eu-TCL1; and 10 months, in which this strain usually develops leukemia. We found that total white blood cells and ercentages of leukemic IgM CD5 cells in PB of DT mice were increased as compared to Eu-TCL1 mice (n=15, p<0.05). DT mice also showed increased liver and spleen sizes, which were highly infiltrated with leukemic B cells. In a long-term follow up survival experiment, DT mice showed a shorter overall survival (median, 308 days) than Eu-TCL1 mice (median, 404 days, p=0.0003). Interestingly, when expression of the proliferation marker Ki-67 was evaluated in leukemic IgM CD5 of PB and spleen, the obtained values were higher in the DT mice at 8 to 10 months of age as compared to the Eu-TCL1 control (n=15, p<0.05 in PB; n=6, p <0.05 in spleen). We conclude that DT mice develop leukemia with more forceful kinetics and aggressiveness compared to Eu-TCL1 mice. We speculate that AID over-expression enhances CLL proliferation by mediating unknown off-target DNA mutations. Identification of AID off-target mutations associated with enhanced proliferation in this model will be evaluated by WES. http://dx.doi.org/10.3109/10428194.2015.1080893
    Leukemia and Lymphoma 09/2015;
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    ABSTRACT: Durable responses to imatinib monotherapy are rarely seen in aggressive forms of Philadelphia chromosome positive (Ph+) leukemias. To investigate the possible cause of treatment failure we examined the role of protein kinase C epsilon (PKCE), an oncogene highly implicated in the development of solid tumors and resistance to chemotherapy. We found high levels of PKCE transcripts in Ph+ acute lymphoblastic leukemia (ALL) cells from patients and cell lines, and imatinib resistant chronic myeloid leukemia, which were also less responsive to imatinib-induced apoptosis than Ph+ cells with lower PKCE expression. Furthermore, the siRNA-mediated knockdown or peptide inhibition of PKCE in Ph+ cells increased imatinib-induced apoptosis while overexpression of PKCE reduced imatinib-induced apoptosis, with concomitant increase in the pro-survival factor AKT. Our results suggest PKCE plays a protective role against apoptosis induced by BCR-ABL inhibition in Ph+ leukemias with high PKCE expression, such as Ph+ ALL.
    Leukemia and Lymphoma 06/2015; DOI:10.3109/10428194.2015.1043545
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    ABSTRACT: The poor treatment response of acute myeloid leukemia (AML) overexpressing high-risk oncogenes such as EVI1, demands specific animal models for new treatment evaluations. Evi1 is a common site of activating integrations in murine leukemia virus (MLV)-induced AML and in retroviral and lentiviral gene-modified HCS. Still, a model of overt AML induced by Evi1 has not been generated. Cell lines from MLV-induced AML are growth factor-dependent and non-transplantable. Hence, for the leukemia maintenance in the infected animals, a growth factor source such as chronic immune response has been suggested. We have investigated whether these leukemias are transplantable if provided with growth factors. We show that the Evi1+DA-3 cells modified to express an intracellular form of GM-CSF, acquired growth factor independence and transplantability and caused an overt leukemia in syngeneic hosts, without increasing serum GM-CSF levels. We propose this as a general approach for modeling different forms of high-risk human AML using similar cell lines.
    Leukemia and Lymphoma 06/2015; DOI:10.3109/10428194.2015.1043547
  • Leukemia and Lymphoma 05/2015;
  • Leukemia and Lymphoma 03/2015; DOI:10.3109/10428194.2015.1028056
  • Leukemia and Lymphoma 03/2015; DOI:10.3109/10428194.2015.1026818
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    ABSTRACT: Optimal conditioning remains a challenge in lymphomas. We designed a regimen, consisting of Busulfex, Etoposide and Melphalan (BuEM). We retrospectively analyzed the outcome of patients conditioned with BEAM or BuEM, in matched-pair analysis on a planned 2:1 ratio. Eighty-seven BEAM patients that fulfilled the matching criteria were randomly selected. Two year PFS/OS were 63.2%/76.7% for BEAM vs 62.0%/77.6% for BuEM after 64.7 and 42.7 months respectively. Furthermore, marginally better PFS and OS was noted in Hodgkin lymphoma (HL) after BuEM. In multivariate analysis, PFS was superior in HL, chemosensitive disease and complete remission post transplantation. BEAM correlated with faster engraftment, reduced infections, less mucositis and liver toxicity; BuEM with less need for blood cell, platelet transfusions and GCSF administration. In conclusion, BuEM was well tolerated and equally, highly efficacious as BEAM for non-Hodgkin lymphoma and offered marginally significant improved PFS and OS in HL with acceptable toxicity and zero mortality.
    Leukemia and Lymphoma 03/2015; DOI:10.3109/10428194.2015.1028054