Claire N Harrison

Guy's and St Thomas' NHS Foundation Trust, Londinium, England, United Kingdom

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Publications (150)1216.68 Total impact

  • Donal P McLornan · Alesia A Khan · Claire N Harrison
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    ABSTRACT: Over the last decade, unparalleled advances have been made within the field of 'Philadelphia chromosome'-negative myeloproliferative neoplasms (MPN) regarding both disease pathogenesis and therapeutic targeting. The discovery of deregulated JAK-STAT signalling in MPN led to the rapid development of JAK inhibitor agents, targeting both mutated and wild-type JAK, which have significantly altered the therapeutic paradigm for patients with MPN. Although the largest population treated with these agents incorporates those with myelofibrosis, increasing data supports potential usage in other MPNs such as essential thromocythaemia and polycythaemia vera. Many MPNs are associated with a hyperinflammatory state and deregulation of immune homeostasis. Over the last few years, research has focused on attempting to decipher the complex and context-dependent changes that contribute to this immune deregulation. Moreover, very recent studies have demonstrated significant JAK inhibitor-mediated effects within the T cell, natural killer cell and dendritic cell compartments following exposure to JAK inhibitors. In parallel, case reports of infections occurring following exposure to ruxolitinib, many of which are atypical, have focused research efforts on delineating JAK inhibitor-associated immunological consequences. Within this review article, we will describe what is currently known about MPN-associated immune deregulation and JAK inhibitor-mediated immunomodulation.
    Current Hematologic Malignancy Reports 08/2015; DOI:10.1007/s11899-015-0284-z · 2.20 Impact Factor
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    ABSTRACT: The aim of this work is to produce recommendations on the management of allogeneic stem cell transplantation (allo-SCT) in primary myelofibrosis (PMF). A comprehensive systematic review of articles released from 1999 to 2015 (January) was used as a source of scientific evidence. Recommendations were produced using a Delphi process involving a panel of 23 experts appointed by the European LeukemiaNet (ELN) and European Blood and Marrow Transplantation Group (EBMT). Key questions included patient selection, donor selection, pre-transplant management, conditioning regimen, post-transplant management, prevention and management of relapse after transplant. Patients with intermediate-2- or high-risk disease and age less than 70 years should be considered candidates for allo-SCT. Patients with intermediate-1-risk disease and age less than 65 years should be considered candidates if they present with either refractory, transfusion-dependent anemia, or a percentage of blasts in peripheral blood greater than 2%, or adverse cytogenetics. Pre-transplant splenectomy should be decided on a case by case basis. Patients with intermediate-2- or high-risk disease lacking an HLA matched sibling or unrelated donor, should be enrolled in a protocol using HLA non-identical donors. Peripheral blood was considered the most appropriate source of hematopoietic stem cells for HLA-matched sibling and unrelated donor transplants. The optimal intensity of the conditioning regimen still needs to be defined. Strategies such as discontinuation of immune-suppressive drugs, donor lymphocyte infusion or both were deemed appropriate to avoid clinical relapse. In conclusion, we provided consensus-based recommendations aimed to optimize allo-SCT in PMF. Unmet clinical needs were highlighted.Leukemia accepted article preview online, 21 August 2015. doi:10.1038/leu.2015.233.
    Leukemia: official journal of the Leukemia Society of America, Leukemia Research Fund, U.K 08/2015; DOI:10.1038/leu.2015.233 · 10.43 Impact Factor
  • Samah Alimam · Donal McLornan · Claire Harrison
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    ABSTRACT: Myelofibrosis is a heterogeneous disorder, which, although sometimes asymptomatic in the early stages, is frequently associated with debilitating constitutional symptoms, poor quality of life and high degree of morbidity as the disease progresses. Ruxolitinib, a JAK1/2-inhibitor, has transformed the management of many patients by reducing disease-related symptoms and splenomegaly in intermediate-2 and high-risk patients. As demonstrated by the COMFORT studies, unprecedented clinical benefit can be gained by some patients on ruxolitinib; however, this is not without potential adverse effects, notably cytopenias, weight-gain and an increased risk of opportunistic infections. No other JAK inhibitors are currently approved for myelofibrosis. Moreover, long-term effects of JAK-inhibitor agents, such as ruxolitinib, remain unknown. Consequently, the use of ruxolitinib in the low-risk patient, in the absence of high symptom burden remains controversial and requires further randomized clinical trials. In such patients, an individualized approach should be adopted, balancing likely clinical benefit with the potential side-effect profile.
    Expert Review of Hematology 08/2015; 8(5):1-3. DOI:10.1586/17474086.2015.1074858 · 2.07 Impact Factor
  • Annals of Oncology 08/2015; 26 Suppl 5. DOI:10.1093/annonc/mdv203 · 7.04 Impact Factor
  • Haematologica 06/2015; 100(9). DOI:10.3324/haematol.2015.128918 · 5.81 Impact Factor
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    ABSTRACT: Myelofibrosis (MF) is a BCR-ABL-negative myeloproliferative neoplasm characterized by anemia, splenomegaly, debilitating constitutional symptoms, and shortened survival. Fedratinib, a JAK2-selective inhibitor, previously demonstrated clinically beneficial activity in patients with MF in early-phase trials. To evaluate the efficacy and safety of fedratinib therapy in patients with primary or secondary (post-polycythemia vera or post-essential thrombocythemia) MF. Double-blind, randomized, placebo-controlled phase 3 study in 94 sites in 24 countries in which 289 adult patients (≥18 years of age) with intermediate-2 or high-risk primary MF, post-polycythemia vera MF, or post-essential thrombocythemia MF were randomly assigned between December 2011 and September 2012 to once-daily oral fedratinib, at a dose of 400 mg or 500 mg, or placebo, for at least 6 consecutive 4-week cycles. The primary end point was spleen response (≥35% reduction in spleen volume from baseline as determined by magnetic resonance imaging or computed tomography) at week 24 and confirmed 4 weeks later. The main secondary end point was symptom response (≥50% reduction in total symptom score, assessed using the modified Myelofibrosis Symptom Assessment Form). The primary end point was achieved by 35 of 96 (36% [95% CI, 27%-46%]) and 39 of 97 (40% [95% CI, 30%-50%]) patients in the fedratinib 400-mg and 500-mg groups, vs 1 of 96 (1% [95% CI, 0%-3%]) in the placebo group (P < .001). Symptom response rates at week 24 were 33 of 91 (36% [95% CI, 26%-46%]), 31 of 91 (34% [95% CI, 24%-44%]), and 6 of 85 (7% [95% CI, 2%-13%]) in the fedratinib 400-mg, 500-mg, and placebo groups, respectively (P < .001). Common adverse events with fedratinib treatment were anemia, gastrointestinal symptoms, and increased levels of liver transaminases, serum creatinine, and pancreatic enzymes. Encephalopathy was reported in 4 women who received fedratinib 500 mg/d. A diagnosis of Wernicke encephalopathy was supported by magnetic resonance imaging in 3 cases and suspected clinically in 1 case. Fedratinib therapy significantly reduced splenomegaly and symptom burden in patients with MF. These benefits were accompanied by toxic effects in some patients, the most important being encephalopathy of unknown mechanism. Clinical development of fedratinib was subsequently discontinued. identifier: NCT01437787.
    06/2015; 1(5). DOI:10.1001/jamaoncol.2015.1590
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    ABSTRACT: CD4(+) T cells maintain cancer surveillance and immune tolerance. Chronic inflammation has been proposed as a driver of clonal evolution in myeloproliferative neoplasms (MPN), suggesting that T cells play an important role in their pathogenesis. Treatment with JAK inhibitors (JAKi) results in improvements in MPN-associated constitutional symptoms as well as reductions in splenomegaly. However, effects of JAKi on T cells in MPN are not well established and the baseline immune signature remains unclear. We investigated the frequency and function of CD4(+) T cell subsets in 50 MPN patients at baseline as well as during treatment with either ruxolitinib or fedratinib in a subset. We show that CD4(+) CD127(low) CD25(high) FOXP3(+) T regulatory cells are reduced in MPN patients compared to healthy controls and that this decrease is even more pronounced following JAKi therapy. Moreover, we show that after 6 months of treatment the number of T helper (Th)-17 cells increased. We also describe a functional 'silencing' of T helper cells both in vivo and in vitro and a blockade of pro-inflammatory cytokines from these cells. This profound effect of JAKi on T cell function may underlay augmented rates of atypical infections that have been reported with use of these drugs. © 2015 John Wiley & Sons Ltd.
    British Journal of Haematology 06/2015; DOI:10.1111/bjh.13519 · 4.71 Impact Factor
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    ABSTRACT: Ruxolitinib, a potent Janus kinase 1/2 inhibitor, resulted in rapid and durable improvements in splenomegaly and disease-related symptoms in the 2 phase 3 COMFORT studies. Additionally, ruxolitinib was associated with prolonged survival compared with placebo (COMFORT-I) and best available therapy (COMFORT-II). We present a pooled analysis of overall survival in the COMFORT studies using an intent-to-treat analysis and an analysis correcting for crossover in the control arms. Overall, 301 patients received ruxolitinib (COMFORT-I, n=155; COMFORT-II, n=146) and 227 patients received placebo (n=154) or best available therapy (n=73). After a median 3 years of follow-up, intent-to-treat analysis showed that patients who received ruxolitinib had prolonged survival compared with patients who received placebo or best available therapy (hazard ratio=0.65; 95% confidence interval, 0.46-0.90; P=.01); the crossover-corrected hazard ratio was 0.29 (95% confidence interval, 0.13-0.63). Both patients with intermediate-2 or high-risk disease showed prolonged survival, and patients with high-risk disease in the ruxolitinib group had survival similar to that of patients with intermediate-2-risk disease in the control group. The Kaplan-Meier estimate of overall survival at week 144 was 78% in the ruxolitinib arm, 61% in the intent-to-treat control arm, and 31% in the crossover-adjusted control arm. While larger spleen size at baseline was prognostic for shortened survival, reductions in spleen size with ruxolitinib treatment correlated with longer survival. These findings are consistent with previous reports and support that ruxolitinib offers a survival benefit for patients with myelofibrosis compared with conventional therapies. ( identifiers: COMFORT-I, NCT00952289; COMFORT-II, NCT00934544). Copyright © 2015, Ferrata Storti Foundation.
    Haematologica 06/2015; 100(9). DOI:10.3324/haematol.2014.119545 · 5.81 Impact Factor
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    ABSTRACT: The present report focuses on management strategies for the myeloproliferative neoplasm according to the structure and processes we use within our center, a large tertiary unit in central London. The standard procedures for achieving an accurate diagnosis and risk stratification and therapeutic strategies for these diseases with a detailed focus on contentious areas are discussed. In the 9 years after the description of the Janus kinase 2 mutation, this field has altered quite radically in several aspects. For example, a new therapeutic paradigm exists, especially for myelofibrosis. We share how our unit has adapted to these changes. Copyright © 2015 Elsevier Inc. All rights reserved.
    Clinical lymphoma, myeloma & leukemia 06/2015; 15S:S19-S26. DOI:10.1016/j.clml.2015.02.032 · 2.02 Impact Factor
  • Alesia A Khan · Claire N Harrison · Donal P McLornan
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    ABSTRACT: Deregulated Hedgehog (Hh) signalling activity may be associated with a broad range of cancer types and hence has become an attractive target for therapeutic intervention. Although initial haematological interest focused on the therapeutic targeting of this pathway in chronic myeloid leukaemia), small molecule inhibitors targeting the Hh pathway are now being tested in a range of other myeloid disorders, including myelofibrosis, myelodysplasia and acute myeloid leukaemia. In this review we will evaluate the rationale for targeting of the Hh pathway in myeloid diseases and discuss the novel agents that have entered the clinical arena. We will discuss pre-clinical models, emerging clinical trial data, and suggest how these targeted therapies may address current unmet medical needs. Finally, we will explore potential limitations of these therapies due to the emergence of secondary resistance mechanisms and speculate on future developments within this arena. © 2015 John Wiley & Sons Ltd.
    British Journal of Haematology 04/2015; 170(3). DOI:10.1111/bjh.13426 · 4.71 Impact Factor
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    ABSTRACT: Myelofibrosis (MF), including primary, post-essential thrombocythemia and post-polycythemia vera MF, associates with a reduced quality of life and shortened life expectancy. Dysregulation of the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway is prominent, even in the absence of the JAK2(V617F) mutation. Therefore, all symptomatic MF patients may potentially derive benefit from JAK inhibitors. Despite the efficacy of JAK inhibitors in controlling signs and symptoms of MF, they do not eradicate the disease. Therefore, JAK inhibitors are currently being tested in combination with other novel therapies, a strategy which may be more effective in reducing disease burden, either by overcoming JAK inhibitor resistance or targeting additional mechanisms of pathogenesis. Additional targets include modulators of epigenetic regulation, pathways that work downstream from JAK/STAT (i.e., mammalian target of rapamycin/AKT/phosphoinositide 3-kinase,) heat shock protein 90, hedgehog signaling, pro-fibrotic factors, abnormal megakaryocytes and telomerase. In this review, we discuss novel MF therapeutic strategies.
    Leukemia & lymphoma 04/2015; DOI:10.3109/10428194.2015.1037762 · 2.89 Impact Factor
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    ABSTRACT: Clonal proliferation in myeloproliferative neoplasms (MPN) is driven by somatic mutations in JAK2, CALR or MPL, but the contribution of inherited factors is poorly characterized. Using a three-stage genome-wide association study of 3,437 MPN cases and 10,083 controls, we identify two SNPs with genome-wide significance in JAK2(V617F)-negative MPN: rs12339666 (JAK2; meta-analysis P=1.27 × 10(-10)) and rs2201862 (MECOM; meta-analysis P=1.96 × 10(-9)). Two additional SNPs, rs2736100 (TERT) and rs9376092 (HBS1L/MYB), achieve genome-wide significance when including JAK2(V617F)-positive cases. rs9376092 has a stronger effect in JAK2(V617F)-negative cases with CALR and/or MPL mutations (Breslow-Day P=4.5 × 10(-7)), whereas in JAK2(V617F)-positive cases rs9376092 associates with essential thrombocythemia (ET) rather than polycythemia vera (allelic χ(2) P=7.3 × 10(-7)). Reduced MYB expression, previously linked to development of an ET-like disease in model systems, associates with rs9376092 in normal myeloid cells. These findings demonstrate that multiple germline variants predispose to MPN and link constitutional differences in MYB expression to disease phenotype.
    Nature Communications 04/2015; 2015(6):6691. DOI:10.1038/ncomms7691 · 11.47 Impact Factor
  • Claire Harrison
    Haematologica 04/2015; 100(4):409-11. DOI:10.3324/haematol.2015.124099 · 5.81 Impact Factor
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    ABSTRACT: Myelofibrosis is characterized by splenomegaly and debilitating constitutional symptoms that negatively impact patients' quality of life. ROBUST, a UK, open-label, phase II study, evaluated the safety and efficacy of ruxolitinib in patients with myelofibrosis (N = 48), including intermediate-1 risk patients. The primary composite endpoint was the proportion of patients achieving treatment success [≥50% reduction in palpable spleen length and/or a ≥50% decrease in Myelofibrosis Symptom Assessment Form Total Symptom Score (MF-SAF TSS)] at 48 weeks. This was the first time that efficacy of ruxolitinib in myelofibrosis has been evaluated based on these criteria and the first time the MF-SAF was used in a population of patients solely from the United Kingdom. Overall, 50% of patients and 57% of intermediate-1 risk patients, achieved treatment success; reductions in spleen length and symptoms were observed in all risk groups. The majority of patients (66·7%) experienced ≥50% reductions from baseline in spleen length at any time. Improvements in MF-SAF TSS were seen in 80·0%, 72·7%, and 72·2% of intermediate-1, intermediate-2, and high-risk patients, respectively. Consistent with other studies of ruxolitinib, the most common haematological adverse events were anaemia and thrombocytopenia. Results indicate that most patients with myelofibrosis, including intermediate-1 risk patients, may benefit from ruxolitinib treatment. © 2015 John Wiley & Sons Ltd.
    British Journal of Haematology 03/2015; 170(1). DOI:10.1111/bjh.13379 · 4.71 Impact Factor
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    ABSTRACT: Cancers result from the accumulation of somatic mutations, and their properties are thought to reflect the sum of these mutations. However, little is known about the effect of the order in which mutations are acquired. We determined mutation order in patients with myeloproliferative neoplasms by genotyping hematopoietic colonies or by means of next-generation sequencing. Stem cells and progenitor cells were isolated to study the effect of mutation order on mature and immature hematopoietic cells. The age at which a patient presented with a myeloproliferative neoplasm, acquisition of JAK2 V617F homozygosity, and the balance of immature progenitors were all influenced by mutation order. As compared with patients in whom the TET2 mutation was acquired first (hereafter referred to as "TET2-first patients"), patients in whom the Janus kinase 2 (JAK2) mutation was acquired first ("JAK2-first patients") had a greater likelihood of presenting with polycythemia vera than with essential thrombocythemia, an increased risk of thrombosis, and an increased sensitivity of JAK2-mutant progenitors to ruxolitinib in vitro. Mutation order influenced the proliferative response to JAK2 V617F and the capacity of double-mutant hematopoietic cells and progenitor cells to generate colony-forming cells. Moreover, the hematopoietic stem-and-progenitor-cell compartment was dominated by TET2 single-mutant cells in TET2-first patients but by JAK2-TET2 double-mutant cells in JAK2-first patients. Prior mutation of TET2 altered the transcriptional consequences of JAK2 V617F in a cell-intrinsic manner and prevented JAK2 V617F from up-regulating genes associated with proliferation. The order in which JAK2 and TET2 mutations were acquired influenced clinical features, the response to targeted therapy, the biology of stem and progenitor cells, and clonal evolution in patients with myeloproliferative neoplasms. (Funded by Leukemia and Lymphoma Research and others.).
    New England Journal of Medicine 02/2015; 372(7):601-12. DOI:10.1056/NEJMoa1412098 · 55.87 Impact Factor
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    ABSTRACT: Ruxolitinib, a Janus kinase (JAK) 1 and 2 inhibitor, was shown to have a clinical benefit in patients with polycythemia vera in a phase 2 study. We conducted a phase 3 open-label study to evaluate the efficacy and safety of ruxolitinib versus standard therapy in patients with polycythemia vera who had an inadequate response to or had unacceptable side effects from hydroxyurea. We randomly assigned phlebotomy-dependent patients with splenomegaly, in a 1:1 ratio, to receive ruxolitinib (110 patients) or standard therapy (112 patients). The primary end point was both hematocrit control through week 32 and at least a 35% reduction in spleen volume at week 32, as assessed by means of imaging. The primary end point was achieved in 21% of the patients in the ruxolitinib group versus 1% of those in the standard-therapy group (P<0.001). Hematocrit control was achieved in 60% of patients receiving ruxolitinib and 20% of those receiving standard therapy; 38% and 1% of patients in the two groups, respectively, had at least a 35% reduction in spleen volume. A complete hematologic remission was achieved in 24% of patients in the ruxolitinib group and 9% of those in the standard-therapy group (P=0.003); 49% versus 5% had at least a 50% reduction in the total symptom score at week 32. In the ruxolitinib group, grade 3 or 4 anemia occurred in 2% of patients, and grade 3 or 4 thrombocytopenia occurred in 5%; the corresponding percentages in the standard-therapy group were 0% and 4%. Herpes zoster infection was reported in 6% of patients in the ruxolitinib group and 0% of those in the standard-therapy group (grade 1 or 2 in all cases). Thromboembolic events occurred in one patient receiving ruxolitinib and in six patients receiving standard therapy. In patients who had an inadequate response to or had unacceptable side effects from hydroxyurea, ruxolitinib was superior to standard therapy in controlling the hematocrit, reducing the spleen volume, and improving symptoms associated with polycythemia vera. (Funded by Incyte and others; RESPONSE number, NCT01243944.).
    New England Journal of Medicine 01/2015; 372(5):426-35. DOI:10.1056/NEJMoa1409002 · 55.87 Impact Factor
  • Claire N Harrison · Natalia Curto Garcia
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    ABSTRACT: Thrombocytosis has a large number of potential underlying causes, but the dominant group of hematological conditions for consideration in this setting are the myeloproliferative neoplasms (MPNs). In this chapter, we consider several key linked questions relating to the management of thrombocytosis in MPNs and discuss several issues. First, we discuss the differential diagnosis of thrombocytosis, which myeloid disorders to consider, and practical approaches to the discrimination of each individual MPN from other causes. Second, there have been several major advances in our understanding of the molecular biology of these conditions and we discuss how these findings are likely to be practically applied in the future. Third, we consider whether there is evidence that thrombocytosis contributes to the complications known to be associated with MPN: thrombosis, hemorrhage and transformation to leukemia and myelofibrosis. Last, we review current ideas for risk stratification and management of essential thrombocythemia and polycythemia vera as the 2 entities within the MPN family that are most frequently associated with thrombocytosis. © 2014 by The American Society of Hematology. All rights reserved.
    Hematology 12/2014; 2014(1):348-54. DOI:10.1182/asheducation-2014.1.348 · 0.81 Impact Factor
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    Claire N Harrison · Mary F McMullin
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    ABSTRACT: The differential diagnosis of haematological abnormalities, such as leucocytosis, erythocytosis, thrombocytosis or indeed anaemia, is wide and disarming. Here we report on significant updates in the differential diagnosis of erythrocyosis and thrombocytosis presenting a simplified schema for the clinician. We then move to discuss significant advances in this field which have followed a series of key molecular findings, most specifically those affecting the JAK/STAT pathway. © 2014 Royal College of Physicians.
    Clinical medicine (London, England) 12/2014; 14 Suppl 6(Suppl_6):s66-70. DOI:10.7861/clinmedicine.14-6-s66 · 1.49 Impact Factor
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    ABSTRACT: Leukemia is one of the leading journals in hematology and oncology. It is published monthly and covers all aspects of the research and treatment of leukemia and allied diseases. Studies of normal hemopoiesis are covered because of their comparative relevance.
    Leukemia 09/2014; 29(3). DOI:10.1038/leu.2014.282 · 10.43 Impact Factor
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    ABSTRACT: The discovery of somatic mutations, primarily JAK2V617F and CALR, in classic BCR-ABL1-negative myeloproliferative neoplasms (MPNs), has generated interest in the development of molecularly targeted therapies, whose accurate assessment requires a standardized framework. A working group, comprised of members from European LeukemiaNet (ELN) and International Working Group for MPN Research and Treatment (IWG-MRT), prepared consensus-based recommendations regarding trial design, patient selection, and definition of relevant endpoints. Accordingly, a response able to capture the long-term effect of the drug should be selected as the endpoint of phase II trials aimed at developing new drugs for MPNs. A time-to-event, such as overall survival, or progression-free survival or both, as co-primary endpoints, should measure efficacy in phase III studies. New drugs should be tested for preventing disease progression in MF patients with early disease in randomized studies, and a time to event, like progression-free or event-free survival should be the primary endpoint. Phase III trials aimed at preventing vascular events in PV and ET should be based on a selection of the target population based on new prognostic factors, including JAK2 mutation. In conclusion, we recommended a format for clinical trials in MPNs which facilitates communication between academic investigators, regulatory agencies and drug companies.Leukemia accepted article preview online, 25 August 2014 doi:10.1038/leu.2014.250.
    Leukemia 08/2014; 29(1). DOI:10.1038/leu.2014.250 · 10.43 Impact Factor

Publication Stats

5k Citations
1,216.68 Total Impact Points


  • 2005–2015
    • Guy's and St Thomas' NHS Foundation Trust
      • Department of Haematology
      Londinium, England, United Kingdom
    • The Bracton Centre, Oxleas NHS Trust
      Дартфорде, England, United Kingdom
    • Ospedali Riuniti di Bergamo
      • Department of Hematology
      Bergamo, Lombardy, Italy
  • 2012
    • Wellcome Trust Sanger Institute
      • Cancer Genome Project
      Cambridge, ENG, United Kingdom
  • 2011
    • Rosalind Franklin University of Medicine and Science
      North Chicago, Illinois, United States
  • 2009
    • Cambridge Institute for Medical Research
      • Department of Haematology
      Cambridge, England, United Kingdom
  • 2005–2009
    • University of Cambridge
      • Department of Haematology
      Cambridge, ENG, United Kingdom
  • 2007
    • Belfast Healthy Cities
      Béal Feirste, N Ireland, United Kingdom
  • 2006
    • Universität Ulm
      Ulm, Baden-Württemberg, Germany
  • 2001
    • University College London
      • Department of Haematology
      Londinium, England, United Kingdom
  • 1998
    • University of Birmingham
      Birmingham, England, United Kingdom