Robert Peter Gale

Imperial College London, Londinium, England, United Kingdom

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Publications (21)90.4 Total impact

  • Jane F Apperley, Robert Peter Gale
    Biology of blood and marrow transplantation: journal of the American Society for Blood and Marrow Transplantation 01/2014; · 3.15 Impact Factor
  • Robert Peter Gale, John M Bennett, F Owen Hoffman
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    ABSTRACT: Therapy-related leukemia or therapy-related myeloid neoplasm are widely-used terms to designate leukemia developing in persons who previously received anti-cancer therapy (for example, see references 1, 2), especially if the prior anti-cancer therapy included drugs such as alkylators, DNA-intercalators, topoisomerase-2-inhibitors, purines and/or ionizing radiation.1 Sometimes specific genes such as AML1, EVI1, NRAS, MLL are mutated in cases of therapy-related leukemia but there are no convincing data the frequency of acquired somatic mutations differs from that of cases not designated as therapy-related. 3 Other cases of therapy-related leukemia have variants of genes (polymorphisms) which inactivate mutagens or repair mutations such as occur in Fanconi anemia (FANC), xeroderma pigmentosa (XPD), NQ01 or AML2 which may increase the risk exposure to potential leukemogenic agents may result in AML. 0020, 0025 and 0030 Recent data suggest an increased frequency of TP53 mutations in cases of therapy-related leukemia but these are likely the result of normal aging rather than exposure to anti-cancer drugs and/or radiation. 7 The issue we address in this commentary is how accurate is the designation of therapy-related AML as commonly used by most hematologists?
    Leukemia research 01/2014; · 2.36 Impact Factor
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    ABSTRACT: Background Anemia is common in myeloproliferative neoplasm (MPN)−associated myelofibrosis. The Functional Assessment of Cancer Therapy (FACT) measurement system is a patient-reported outcomes instrument that documents symptoms of the diverse aspects of cancer treatment. One FACT version, FACT-Anemia (FACT-An), documents symptoms of anemia related to cancer. The FACT-An has been validated in diverse cancer populations, but not in MPN-associated myelofibrosis. Objective Our aim was to evaluate the relationship between anemia response to therapy with pomalidomide with or without corticosteroids and patient-reported outcomes using the FACT-An instrument. Methods Data were obtained from a Phase II, randomized, double-blind Bayesian pick-the-winner trial of prednisone and pomalidomide in patients with MPN-associated myelofibrosis and anemia (red blood cell−transfusion dependence). Details of the study, including definitions of anemia, anemia response, red blood cell−transfusion, red blood cell−transfusion dependence, and red blood cell−transfusion independence, are reported. Change in quality of life from randomization to the last cycle of therapy was evaluated using the FACT-An Physical Well Being, Functional Well Being, Trial Outcome Index, and Anemia domains. Clinically important differences were used to determine the smallest difference in scores that patients perceived as beneficial in the FACT-An domains of interest. Patients were classified as meeting clinically important differences for responsiveness if their change score from baseline was >1 SEM, indicating improvement. Results Eighty-five patients were studied. Thirty-one patients (37%) were classified as anemia responders by prospectively defined criteria. Across all FACT-An domains, anemia responders showed greater improvement in Physical Well Being, Functional Well Being, and Trial Outcome Index scores than did nonresponders. This improvement began at the second 28-day cycle of therapy and was sustained. Conclusions We show a correlation between anemia response and improved quality of life measured by the FACT-An instrument in patients with MPN-associated myelofibrosis and anemia.
    Clinical Therapeutics 01/2014; · 2.23 Impact Factor
  • Robert Peter Gale
    Biology of blood and marrow transplantation: journal of the American Society for Blood and Marrow Transplantation 05/2013; · 3.15 Impact Factor
  • S Hudgens, R P Gale, T Tencer, Z Khan
    Value in Health 05/2013; 16(3):A148. · 2.19 Impact Factor
  • Robert Peter Gale
    Leukemia: official journal of the Leukemia Society of America, Leukemia Research Fund, U.K 02/2013; 27(2):259. · 10.16 Impact Factor
  • Leukemia research 02/2012; 36(5):659-60. · 2.36 Impact Factor
  • Giovanni Barosi, Robert Peter Gale
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    ABSTRACT: The dominant pathophysiological and clinical features of myeloproliferative neoplasm (MPN)-associated myelofibrosis are caused by bone marrow fibrosis. It is widely believed this fibrosis is a reaction to the MPN-clone implying the cells causing fibrosis are polyclonal and genetically unrelated to the MPN-clone. We cite recent data illustrating the complexity of cell types comprising the bone marrow micro-environment and showing that at least some of the cells responsible for bone marrow fibrosis are clonal and genetically related to the MPN-clone.
    Leukemia research 02/2011; 35(5):563-5. · 2.36 Impact Factor
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    ABSTRACT: The term RBC-transfusion-dependence is widely-used by hematologists to describe a condition of severe anemia typically arising when erythropoiesis is reduced such that a person continuously requires ≥1 RBC-transfusions over a specified interval. Defining a person as RBC-transfusion-dependent has important implications in diverse hematological disorders especially because it strongly-correlated with decreased survival. Conversely, becoming RBC-transfusion-independent or receiving fewer RBC-transfusions over a specified interval is defined as improvement or response in many disease- and/or therapy-setting. Whether this correlates with improved survival is controversial. We used a structured expert-panel consensus panel process to define RBC-transfusion-dependence and -independence or improvement. We suggest these definitions may prove useful to persons studying or treating these diseases.
    Leukemia research 01/2011; 35(1):8-11. · 2.36 Impact Factor
  • Source
    Chaim Hershko, Robert Peter Gale
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    ABSTRACT: Iron overload in myelodysplastic syndrome (MDS) results from multiple RBC-transfusions and inappropriate increased iron absoption associated with ineffective erythropoiesis. Data from hereditary iron-loading anemias indicate long-term consequences of iron toxicity are preventable and potentially reversible by effective iron-chelation therapy (ICT). There is increasing interest in using ICT in persons with MDS because of the recent introduction of orally effective iron-chelators which are suitable for older persons. Ideally, opinions supporting the benefit of ICT in MDS should be evidenced-based, especially data from randomized trials showing better survival and, in exceptional cases, improved heart function. Such data are lacking. Nevertheless, it is possible to rely on the extensive data from trials of ICT in per-sons with thalassemia and to use well-defined predictors of increased risks of life-threatening complications to identify persons with MDS most likely to benefit from ICT.
    Open Journal of Blood Diseases. 01/2011; 1.
  • Source
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    ABSTRACT: This review focuses on topical issues in the biology and treatment of the myeloproliferative neoplasms (MPNs). Studies in transgenic mice suggest that BCR-ABL1 reduces the fraction of self-renewing 'leukemic' stem cells in the bone marrow but that some of these cells survive treatment with imatinib. This also seems to operate in humans. Data from models also strongly support the notion that JAK2(V617F) can initiate and sustain MPNs in mice; relevance to disease in humans is less clear. These data also support the hypothesis that level of JAK2(V617F) expression influences the MPN phenotype: higher levels favor erythrocytosis whereas lower levels favor thrombocytosis. Although TET2-mutations were thought to precede JAK2(V617F) in some persons with MPNs, it now appears that TET2 mutations may occur after JAK2(V617F). Further understanding of signal-transduction pathways activated in chronic myeloid leukemia suggests various possible targets for new therapies including the WNT/beta catenin, notch and hedgehog pathways. Finally, the clinical role of the new JAK2- and BCR-ABL1-inhibitors is considered. Much further progress is likely in several of these areas soon.
    Haematologica 01/2011; 96(4):590-601. · 5.94 Impact Factor
  • Leukemia research 01/2011; 35(1):12-3. · 2.36 Impact Factor
  • Giovanni Barosi, Umberto Magrini, Robert Peter Gale
    Leukemia research 09/2010; 34(9):1119-20. · 2.36 Impact Factor
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    ABSTRACT: Thalidomide and lenalidomide can alleviate anemia in myelofibrosis. However, their value is undermined by their respective potential to cause peripheral neuropathy and myelosuppression. We therefore evaluated the safety and therapeutic activity of another immunomodulatory drug, pomalidomide. In a phase II randomized, multicenter, double-blind, adaptive design study, four treatment arms were evaluated: pomalidomide (2 mg/d) plus placebo, pomalidomide (2 mg/d) plus prednisone, pomalidomide (0.5 mg/d) plus prednisone, and prednisone plus placebo. Pomalidomide was administered for up to 12 28-day treatment cycles. Prednisone (30 mg/d) was given in a tapering dose schedule during the first three cycles. Response was assessed by International Working Group criteria. Eighty-four patients with myelofibrosis-associated anemia were randomly assigned to the aforementioned treatment arms: 22, 19, 22, and 21, respectively. Response in anemia was documented in 20 patients, including 15 who became transfusion independent. Response rates in the four treatment arms were 23% (95% CI, 5% to 41%), 16% (95% CI, 0% to 33%), 36% (95% CI, 16% to 56%), and 19% (95% CI, 2% to 36%). The corresponding figures for patients receiving > or = 3 cycles of treatment (n = 62) were 38%, 23%, 40%, and 25%. Response to pomalidomide with or without prednisone was durable (range, 3.2 to 16.9+ months) and significantly better in the absence of leukocytosis (37% v 8%; P = .01); JAK2V617F or cytogenetic status did not affect response. Grade > or = 3 toxicities were infrequent and included (in each treatment arm) neutropenia (9%; 16%; 5%; 5%), thrombocytopenia (14%; 16%; 9%; 5%), and thrombosis (9%; 5%; 0%; 0%). Pomalidomide therapy at 0.5 or 2 mg/d with or without an abbreviated course of prednisone is well tolerated in patients with myelofibrosis and active in the treatment of anemia.
    Journal of Clinical Oncology 09/2009; 27(27):4563-9. · 18.04 Impact Factor
  • Ruben Mesa, Robert Peter Gale
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    ABSTRACT: JAK2-inhibitors rapidly reduce spleen enlargement and clinical symptoms in persons with myelofibrosis but have little, if any, effect on the WBC, anemia, decreased platelets or bone marrow fibrosis. Also, JAK2-inhibitors are active in persons with and without the JAK2-mutation. Based on these and other data we suggest that the predominant effect of JAK2-inhibitors in persons with myelofibrosis is on normal rather than the abnormal clones.
    Leukemia research 06/2009; 33(9):1156-7. · 2.36 Impact Factor
  • Robert Peter Gale, John M Bennett
    Leukemia research 12/2008; 33(3):351-4. · 2.36 Impact Factor
  • Robert Peter Gale, Isaac Ben Bassat
    British Journal of Haematology 07/2008; 65(3):261 - 264. · 4.94 Impact Factor
  • Chaim Hershko, Robert Peter Gale, Winston Ho, John Fitchen
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    ABSTRACT: We studied the role of ABH antigens in determining graft outcome in 104 patients who received HLA-identical bone marrow transplants for aplastic anaemia and acute leukaemia. ABH compatibility had no significant effect on incidence of graft rejection or graft-versus-host disease. Fifteen recipients had pre-transplant antibodies against donor ABH antigens. In 14, large volume plasma exchange and transfusion of donor-type erythrocytes was successful in reducing the antibody titre to low or undetectable levels. In one patient, plasma exchange was unsuccessful and red cells were removed from the marrow inoculum by unit gravity sedimentation. This approach prevented transfusion reaction, and permitted engraftment of all haematopoietic cell lines despite persistently elevated antibody titres. Parallel in vitro studies revealed that antibodies to ABH antigens failed to inhibit the growth of progenitor cells committed to both granulocyte-macrophage (CFU-C) and erythroid (BFU-E) development. These findings indicate that ABH-antigens are not clinically important transplantation antigens and suggest that ABH antigens are not operationally present on hematopoietic stem cells.
    British Journal of Haematology 03/2008; 44(1):65 - 73. · 4.94 Impact Factor
  • Robert Peter Gale
    Immunological Reviews 04/2006; 88(1):193 - 214. · 12.16 Impact Factor
  • Robert Peter Gale
    Immunologic Research 1(1):40-66. · 2.96 Impact Factor

Publication Stats

167 Citations
90.40 Total Impact Points


  • 2009–2014
    • Imperial College London
      • • Department of Medicine
      • • Division of Experimental Medicine
      Londinium, England, United Kingdom
  • 2011
    • Policlinico San Matteo Pavia Fondazione IRCCS
      Ticinum, Lombardy, Italy
    • Shaare Zedek Medical Center
      • Department of Hematology
      Yerushalayim, Jerusalem District, Israel
  • 2009–2011
    • Mayo Clinic - Scottsdale
      Scottsdale, Arizona, United States
  • 2006
    • University of California, Los Angeles
      • Department of Medicine
      Los Angeles, CA, United States