Junia V Melo

Summary

Affiliation: Imperial College
Country: UK

Publications

  1. ncbi request reprint Resistance to imatinib mesylate in chronic myeloid leukaemia
    Junia V Melo
    Department of Haematology, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 0NN, United Kingdom
    Cancer Lett 249:121-32. 2007
  2. ncbi request reprint Chronic myeloid leukaemia as a model of disease evolution in human cancer
    Junia V Melo
    Department of Haematology, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK
    Nat Rev Cancer 7:441-53. 2007
  3. ncbi request reprint Biology of chronic myelogenous leukemia--signaling pathways of initiation and transformation
    Junia V Melo
    Department of Haematology, Imperial College, London and Hammersmith Hospital, Du Cane Road, London W12 0NN, UK
    Hematol Oncol Clin North Am 18:545-68, vii-viii. 2004
  4. ncbi request reprint Bcr-Abl expression levels determine the rate of development of resistance to imatinib mesylate in chronic myeloid leukemia
    David J Barnes
    Department of Haematology, Faculty of Medicine, Imperial College London, Hammersmith Hospital, London, United Kingdom
    Cancer Res 65:8912-9. 2005
  5. ncbi request reprint Association between BMI-1 expression, acute graft-versus-host disease, and outcome following allogeneic stem cell transplantation from HLA-identical siblings in chronic myeloid leukemia
    Mohamad Mohty
    Department of Haematology, Imperial College London, Hammersmith Hospital, London, United Kingdom
    Blood 112:2163-6. 2008
  6. doi request reprint BCR-ABL in chronic myelogenous leukemia--how does it work?
    John M Goldman
    Department of Haematology, Imperial College at Hammersmith Hospital, London, UK
    Acta Haematol 119:212-7. 2008
  7. ncbi request reprint The polycomb group BMI1 gene is a molecular marker for predicting prognosis of chronic myeloid leukemia
    Mohamad Mohty
    Department of Hematology, Imperial College London, Hammersmith Hospital, London, United Kingdom
    Blood 110:380-3. 2007
  8. ncbi request reprint In search of the original leukemic clone in chronic myeloid leukemia patients in complete molecular remission after stem cell transplantation or imatinib
    Manuel Sobrinho-Simoes
    Department of Haematology, Imperial College London, London, United Kingdom
    Blood 116:1329-35. 2010
  9. ncbi request reprint Comparative gene expression profile of chronic myeloid leukemia cells innately resistant to imatinib mesylate
    Alex J Tipping
    Department of Haematology, Imperial College London, Hammersmith Hospital, London, UK
    Exp Hematol 31:1073-80. 2003
  10. ncbi request reprint Biology of chronic myeloid leukemia and possible therapeutic approaches to imatinib-resistant disease
    Chikashi Yoshida
    Department of Haematology, Imperial College London, Hammersmith Hospital, London, United Kingdom
    Int J Hematol 79:420-33. 2004

Collaborators

Detail Information

Publications47

  1. ncbi request reprint Resistance to imatinib mesylate in chronic myeloid leukaemia
    Junia V Melo
    Department of Haematology, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 0NN, United Kingdom
    Cancer Lett 249:121-32. 2007
    ..Two such compounds are now being explored in clinical trials. This review will describe the molecular basis of imatinib-resistance and strategies to overcome resistance...
  2. ncbi request reprint Chronic myeloid leukaemia as a model of disease evolution in human cancer
    Junia V Melo
    Department of Haematology, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK
    Nat Rev Cancer 7:441-53. 2007
    ..The causes of this transformation are still poorly understood. What mechanisms underlie this progression, and are they shared by other common cancers?..
  3. ncbi request reprint Biology of chronic myelogenous leukemia--signaling pathways of initiation and transformation
    Junia V Melo
    Department of Haematology, Imperial College, London and Hammersmith Hospital, Du Cane Road, London W12 0NN, UK
    Hematol Oncol Clin North Am 18:545-68, vii-viii. 2004
    ..CML is subject to an inexorable progression from an "indolent" chronic phase to a terminal blast crisis. Disease progression is presumed to be associated with the phenomenon of genomic instability...
  4. ncbi request reprint Bcr-Abl expression levels determine the rate of development of resistance to imatinib mesylate in chronic myeloid leukemia
    David J Barnes
    Department of Haematology, Faculty of Medicine, Imperial College London, Hammersmith Hospital, London, United Kingdom
    Cancer Res 65:8912-9. 2005
    ....
  5. ncbi request reprint Association between BMI-1 expression, acute graft-versus-host disease, and outcome following allogeneic stem cell transplantation from HLA-identical siblings in chronic myeloid leukemia
    Mohamad Mohty
    Department of Haematology, Imperial College London, Hammersmith Hospital, London, United Kingdom
    Blood 112:2163-6. 2008
    ..3-6.4; P = .011), suggesting that BMI-1 measured prior to allo-SCT can serve as a biomarker for predicting outcome in patients with CP-CML receiving allo-SCT, and may thus contribute to better therapeutic decisions...
  6. doi request reprint BCR-ABL in chronic myelogenous leukemia--how does it work?
    John M Goldman
    Department of Haematology, Imperial College at Hammersmith Hospital, London, UK
    Acta Haematol 119:212-7. 2008
    ....
  7. ncbi request reprint The polycomb group BMI1 gene is a molecular marker for predicting prognosis of chronic myeloid leukemia
    Mohamad Mohty
    Department of Hematology, Imperial College London, Hammersmith Hospital, London, United Kingdom
    Blood 110:380-3. 2007
    ..001). We conclude that BMI1 may be a biomarker for the intrinsic heterogeneity of CML, and its measurement at diagnosis can help predict overall survival and thus contribute to better therapeutic decisions...
  8. ncbi request reprint In search of the original leukemic clone in chronic myeloid leukemia patients in complete molecular remission after stem cell transplantation or imatinib
    Manuel Sobrinho-Simoes
    Department of Haematology, Imperial College London, London, United Kingdom
    Blood 116:1329-35. 2010
    ..Post-SCT, we found little evidence that the transcripts occasionally detected originate from the leukemic clone...
  9. ncbi request reprint Comparative gene expression profile of chronic myeloid leukemia cells innately resistant to imatinib mesylate
    Alex J Tipping
    Department of Haematology, Imperial College London, Hammersmith Hospital, London, UK
    Exp Hematol 31:1073-80. 2003
    ..However, in a proportion of patients neither mechanism operates, and resistance appears to be a priori, existing prior to exposure to the drug. These mechanisms of imatinib resistance are poorly understood and may be heterogeneous...
  10. ncbi request reprint Biology of chronic myeloid leukemia and possible therapeutic approaches to imatinib-resistant disease
    Chikashi Yoshida
    Department of Haematology, Imperial College London, Hammersmith Hospital, London, United Kingdom
    Int J Hematol 79:420-33. 2004
    ..Further investigations into the molecular mechanisms of disease and how to specifically target the abnormal processes will guide the design of new treatment modalities in future clinical trials...
  11. ncbi request reprint Imatinib mesylate at therapeutic doses has no impact on folliculogenesis or spermatogenesis in a leukaemic mouse model
    Beate Schultheis
    Department of Haematology, Imperial College and Hammersmith Hospital, London, UK
    Leuk Res 36:271-4. 2012
    ..No effects on folliculogenesis or spermatogenesis could be observed postmortem by histological examinations, suggesting that, at least in two mouse models of imatinib treatment this tyrosine kinase inhibitor does not reduce fertility...
  12. ncbi request reprint Response to imatinib mesylate in patients with chronic myeloproliferative diseases with rearrangements of the platelet-derived growth factor receptor beta
    Jane F Apperley
    Department of Haematology, Faculty of Medicine, Imperial College, Hammersmith Hospital, London, United Kingdom
    N Engl J Med 347:481-7. 2002
    ..The tyrosine kinase inhibitor imatinib mesylate specifically inhibits ABL, PDGFR, and KIT kinases and has impressive clinical efficacy in BCR-ABL-positive chronic myeloid leukemia...
  13. ncbi request reprint Primitive, quiescent and difficult to kill: the role of non-proliferating stem cells in chronic myeloid leukemia
    David J Barnes
    Department of Haematology, Imperial College London, Hammersmith Hospital, London, UK
    Cell Cycle 5:2862-6. 2006
    ..We also discuss possible alternative, Bcr-Abl-independent, mechanisms for the insensitivity of these cells to agents which promote apoptosis, including the putative role of transporter proteins in causing abnormal drug influx or efflux...
  14. ncbi request reprint Molecular profiling of CD34+ cells identifies low expression of CD7, along with high expression of proteinase 3 or elastase, as predictors of longer survival in patients with CML
    Agnes S M Yong
    Department of Haematology, Imperial College London, Hammersmith Hospital, Du Cane Rd, London W12 0NN, United Kingdom
    Blood 107:205-12. 2006
    ....
  15. doi request reprint CD40 and B-cell receptor signalling induce MAPK family members that can either induce or repress Bcl-6 expression
    Ana Batlle
    Department of Haematology, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK
    Mol Immunol 46:1727-35. 2009
    ..We demonstrate for the first time that p38 induces Bcl-6 transcription, but increased protein expression occurs only when the strong pathways repressing Bcl-6 are not activated...
  16. ncbi request reprint Chronic myeloid leukemia--advances in biology and new approaches to treatment
    John M Goldman
    Department of Haematology, Faculty of Medicine, Hammersmith Hospital, Imperial College London, London, United Kingdom
    N Engl J Med 349:1451-64. 2003
  17. ncbi request reprint Overexpression of SOCS-2 in advanced stages of chronic myeloid leukemia: possible inadequacy of a negative feedback mechanism
    Beate Schultheis
    Department of Haematology, Faculty of Medicine, Imperial College of Science, Technology and Medicine, London, United Kingdom
    Blood 99:1766-75. 2002
    ..Overall, the results suggest that SOCS-2 is a component of a negative feedback mechanism; it is induced by Bcr-Abl but cannot reverse its overall growth-promoting effects in blastic transformation...
  18. ncbi request reprint Management of chronic myeloid leukemia: targets for molecular therapy
    David J Barnes
    Department of Haematology, Faculty of Medicine, Imperial College of Science, Technology and Medicine, Hammersmith Hospital, London, UK
    Semin Hematol 40:34-49. 2003
    ..Furthermore, it is believed that Bcr-Abl continues to play a central role throughout the course of the disease...
  19. ncbi request reprint Dose-dependent effects of Bcr-Abl in cell line models of different stages of chronic myeloid leukemia
    David J Barnes
    Department of Haematology, Faculty of Medicine, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK
    Oncogene 24:6432-40. 2005
    ..These findings suggest that the level of Bcr-Abl may be essential in determining the phenotype of the leukemic clone at different stages of the disease...
  20. ncbi request reprint Bcr-Abl signaling through the PI-3/S6 kinase pathway inhibits nuclear translocation of the transcription factor Bach2, which represses the antiapoptotic factor heme oxygenase-1
    Chikashi Yoshida
    Department of Haematology, Imperial College London, Hammersmith Hospital, UK
    Blood 109:1211-9. 2007
    ....
  21. ncbi request reprint Cytogenetic and molecular genetic aspects of chronic myeloid leukaemia
    David J Barnes
    Department of Haematology, Faculty of Medicine, Imperial College of Science, Technology and Medicine, Hammersmith Hospital, London, UK
    Acta Haematol 108:180-202. 2002
    ..CML is subject to an inexorable progression from an 'indolent' chronic phase to a terminal blast crisis. Disease progression is presumed to be associated with the phenomenon of genomic instability...
  22. ncbi request reprint Allorestricted cytotoxic T cells specific for human CD45 show potent antileukemic activity
    Persis J Amrolia
    Department of Haematology, Imperial College School of Medicine, London, United Kingdom
    Blood 101:1007-14. 2003
    ..Further, because P1218-specific CTLs also recognize healthy HLA-A2(+) progenitors, such CTLs could also contribute to host myeloablation and enhance donor cell engraftment...
  23. ncbi request reprint Imatinib mesylate in combination with other chemotherapeutic drugs: in vitro studies
    Alex J Tipping
    Department of Haematology, Imperial College London, Hammersmith Hospital, London, UK
    Semin Hematol 40:83-91. 2003
    ..These represent regimens where imatinib is combined with conventional chemotherapeutic drugs or with inhibitors of other key signal transduction molecules that may be preferentially activated in CML cells...
  24. ncbi request reprint Comparative gene expression profile of p185(Bcr-Abl) versus p210(Bcr-Abl) expressing cells
    Alex J Tipping
    Leuk Res 28:219-20. 2004
  25. ncbi request reprint Upregulation of the TGFbeta signalling pathway by Bcr-Abl: implications for haemopoietic cell growth and chronic myeloid leukaemia
    Gigi M O Møller
    School of Biological Sciences, University of East Anglia, Norwich NR4 7TJ, UK
    FEBS Lett 581:1329-34. 2007
    ....
  26. ncbi request reprint Enhanced Bcr-Abl-specific antileukemic activity of arsenic trioxide (Trisenox) through glutathione-depletion in imatinib-resistant cells
    Heiko Konig
    III Medizinische Klinik, Medizinische Fakultat Mannheim, Universitat Heidelberg, Mannheim, Germany
    Haematologica 92:838-41. 2007
    ..These data provide a rationale for the clinical development of optimized ATO-based regimens through incorporation of GSH-modulators in CML treatment...
  27. ncbi request reprint The use of isobaric tag peptide labeling (iTRAQ) and mass spectrometry to examine rare, primitive hematopoietic cells from patients with chronic myeloid leukemia
    Stephen D Griffiths
    Division of Cancer Studies, Faculty of Medical and Human Sciences, Christie Hospital, University of Manchester, Wilmslow Road, Manchester M20 9BX, UK
    Mol Biotechnol 36:81-9. 2007
    ..DEAD-box protein 3, heat shock protein 105 kDa, and peroxiredoxin-3 were identified as potential protein markers for response to imatinib...
  28. ncbi request reprint Analysis of total phosphotyrosine levels in CD34+ cells from CML patients to predict the response to imatinib mesylate treatment
    Beate Schultheis
    Blood 105:4893-4. 2005
  29. ncbi request reprint Mutation in the ATP-binding site of BCR-ABL in a patient with chronic myeloid leukaemia with increasing resistance to STI571
    Christophe Barthe
    Laboratoire de Greffe de Moelle et Laboratoire d hématologie, Université Victor Segalen and Service des Maladies du Sang, CHU de Bordeaux, Bordeaux, France
    Br J Haematol 119:109-11. 2002
    ..We suggest that the acquisition of point-mutations in the tyrosine kinase domain of Bcr-Abl may cause progressive clinical resistance to STI571...
  30. ncbi request reprint Acquired resistance to imatinib mesylate: selection for pre-existing mutant cells
    Lucio Luzzatto
    Blood 100:1105. 2002
  31. ncbi request reprint Overcoming STI571 resistance with the farnesyl transferase inhibitor SCH66336
    Russell R Hoover
    Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA
    Blood 100:1068-71. 2002
    ..Our data provide a rationale for combination clinical trials of STI571 and SCH66336 in CML patients and suggest that combination therapy may be effective in patients with STI571 resistance...
  32. ncbi request reprint Transient response to imatinib mesylate (STI571) in a patient with the ETV6-ABL t(9;12) translocation
    Stephen G O'Brien
    School of Clinical and Laboratory Sciences and the School of Biochemistry and Genetics, University of Newcastle, United Kingdom
    Blood 99:3465-7. 2002
    ..This case has implications for the design of future studies using STI571 in leukemias involving ABL-encoded fusion proteins other than BCR-ABL...
  33. ncbi request reprint Novel compounds with antiproliferative activity against imatinib-resistant cell lines
    Enrica I Lerma
    Sidney Kimmel Cancer Center, 10835 Altman Row, San Diego, CA 92121, USA
    Mol Cancer Ther 6:655-66. 2007
    ..Some of these drugs were potent inhibitors not only of Abl tyrosine kinase but also of the Src, Lyn, and Fyn tyrosine kinases...
  34. ncbi request reprint Imatinib mesylate (STI-571) reduces Bcr-Abl-mediated vascular endothelial growth factor secretion in chronic myelogenous leukemia
    John M L Ebos
    Molecular and Cell Biology Research, Sunnybrook and Women s College Health Sciences Centre, Toronto, Ontario, Canada M4N 3M5
    Mol Cancer Res 1:89-95. 2002
    ..Taken together, our results implicate BCR-ABL as a possible regulator of CML angiogenesis and raise the possibility that STI-571 could mediate some of its anti-CML properties in vivo through an angiogenesis-dependent mechanism...
  35. ncbi request reprint Antileukemic activity of lysophosphatidic acid acyltransferase-beta inhibitor CT32228 in chronic myelogenous leukemia sensitive and resistant to imatinib
    Paul La Rosée
    Division of Hematology and Medical Oncology, Oregon Health and Sciences University, Portland, Oregon
    Clin Cancer Res 12:6540-6. 2006
    ..Inhibition of LPAAT-beta induces growth arrest and apoptosis in cancer cell lines, implicating LPAAT-beta as a potential drug target in neoplasia...
  36. pmc Modulation of the p38 MAPK (mitogen-activated protein kinase) pathway through Bcr/Abl: implications in the cellular response to Ara-C
    Víctor Javier Sánchez-Arévalo Lobo
    Immunology Department, Hospital Universitario Puerta de Hierro, 28035 Madrid, Spain
    Biochem J 387:231-8. 2005
    ..Our results demonstrate that the involvement of Bcr/Abl in the p38 MAPK pathway is a key mechanism for explaining resistance to Ara-C, and could provide a clue for new therapeutic approaches based on the use of specific Abl inhibitors...
  37. ncbi request reprint Overproduction of BCR-ABL induces apoptosis in imatinib mesylate-resistant cell lines
    Vanessa Desplat
    Laboratoire Hematopoïése normale et pathologique FRE CNRS 2617, Universite Victor Segalen, Bordeaux Cedex, France
    Cancer 103:102-10. 2005
    ..Resistance to imatinib is currently the most important concern of this treatment. One of the main mechanisms of this resistance is overexpression of BCR-ABL...
  38. ncbi request reprint Bcr-Abl kinase modulates the translation regulators ribosomal protein S6 and 4E-BP1 in chronic myelogenous leukemia cells via the mammalian target of rapamycin
    Chi Ly
    Division of Hematology Oncology, Department of Medicine, College of Medicine, University of California, Irvine, California 92697, USA
    Cancer Res 63:5716-22. 2003
    ..The mTOR inhibitor rapamycin enhanced imatinib-mediated killing of CML cell lines in vitro, and it overcame imatinib resistance in cells with Bcr-Abl gene amplification...
  39. ncbi request reprint In vitro efficacy of combined treatment depends on the underlying mechanism of resistance in imatinib-resistant Bcr-Abl-positive cell lines
    Paul La Rosée
    Oregon Health and Science University Cancer Institute, Division of Hematology and Medical Oncology, Portland, OR 97239, USA
    Blood 103:208-15. 2004
    ..These data underline the importance of resistance testing and provide a rational approach for dose-adjusted administration of imatinib when combined with other agents...
  40. ncbi request reprint A novel K509I mutation of KIT identified in familial mastocytosis-in vitro and in vivo responsiveness to imatinib therapy
    Ling Yan Zhang
    Wessex Regional Genetics Laboratory, Salisbury, UK
    Leuk Res 30:373-8. 2006
    ..Mutation analysis of the KIT coding region in this family identified a novel A>T mutation at nucleotide 1547 [K509I] in exon 9 in both of the affected patients...
  41. ncbi request reprint Cross-resistance of imatinib mesylate and 17-AAG in imatinib-resistant cells that overexpress BCR-ABL
    Julian Topaly
    Br J Haematol 121:672-3. 2003
  42. ncbi request reprint Mutations of the myeloid transcription factor CEBPA are not associated with the blast crisis of chronic myeloid leukaemia
    Thomas Pabst
    Institute of Medical Oncology, University Hospital, Berne, Switzerland
    Br J Haematol 133:400-2. 2006
    ..Here, no CEBPA mutation in 95 CML-BC patients was found, suggesting a limited role, if any, of CEBPA mutations in this disorder...
  43. ncbi request reprint MDR1 gene overexpression confers resistance to imatinib mesylate in leukemia cell line models
    Francois Xavier Mahon
    Laboratoire Greffe de Moelle, Universite Victor Segalen, Bordeaux, France
    Blood 101:2368-73. 2003
    ..The possible role of MDR overexpression in clinical resistance to imatinib remains to be defined. We therefore confirm that imatinib should be added to the extensive list of drugs that can be affected by the MDR phenomenon...
  44. ncbi request reprint Imatinib: can one outwit chronic myeloid leukemia?
    Lucio Luzzatto
    Haematologica 87:898-901. 2002
  45. ncbi request reprint Nuclear positioning of the BACH2 gene in BCR-ABL positive leukemic cells
    Atsushi Ono
    Department of Cellular Biology, Research Institute for Radiation Biology and Medicine, Graduate School of Biomedical Science, Hiroshima University, Hiroshima, Japan
    Genes Chromosomes Cancer 46:67-74. 2007
    ....
  46. ncbi request reprint Inactivation of HOXA genes by hypermethylation in myeloid and lymphoid malignancy is frequent and associated with poor prognosis
    Gordon Strathdee
    Centre for Oncology and Applied Pharmacology, Cancer Research UK
    Clin Cancer Res 13:5048-55. 2007
    ..We aimed to study the role of DNA methylation as an inducer of HOX gene silencing in leukemia...
  47. ncbi request reprint Production of P-glycoprotein from the MDR1 upstream promoter is insufficient to affect the response to first-line chemotherapy in advanced breast cancer
    Selina Raguz
    Medical Research Council Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Hospital Campus, London, United Kingdom
    Int J Cancer 122:1058-67. 2008
    ....