Research Topics
Genomes and GenesSpecies | Junia V MeloSummaryAffiliation: Imperial College Country: UK Publications
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Publications
Resistance to imatinib mesylate in chronic myeloid leukaemiaJunia 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...- Biology of chronic myelogenous leukemia--signaling pathways of initiation and transformationJunia 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... - Chronic myeloid leukaemia as a model of disease evolution in human cancerJunia 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?.. - Bcr-Abl expression levels determine the rate of development of resistance to imatinib mesylate in chronic myeloid leukemiaDavid J Barnes
Department of Haematology, Faculty of Medicine, Imperial College London, Hammersmith Hospital, London, United Kingdom
Cancer Res 65:8912-9. 2005.... - Association between BMI-1 expression, acute graft-versus-host disease, and outcome following allogeneic stem cell transplantation from HLA-identical siblings in chronic myeloid leukemiaMohamad 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... - The polycomb group BMI1 gene is a molecular marker for predicting prognosis of chronic myeloid leukemiaMohamad 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... - 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.... - Comparative gene expression profile of chronic myeloid leukemia cells innately resistant to imatinib mesylateAlex J Tipping
Department of Haematology, Imperial College London, Hammersmith Hospital, London, UK
Exp Hematol 31:1073-80. 2003..Given the high rate of primary imatinib resistance in blast crisis, the potential of activating such alternative pathways appears to correlate with disease progression... - In search of the original leukemic clone in chronic myeloid leukemia patients in complete molecular remission after stem cell transplantation or imatinibManuel 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... - Biology of chronic myeloid leukemia and possible therapeutic approaches to imatinib-resistant diseaseChikashi 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... - Primitive, quiescent and difficult to kill: the role of non-proliferating stem cells in chronic myeloid leukemiaDavid 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... - 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 CMLAgnes S M Yong
Department of Haematology, Imperial College London, Hammersmith Hospital, Du Cane Rd, London W12 0NN, United Kingdom
Blood 107:205-12. 2006.... - CD40 and B-cell receptor signalling induce MAPK family members that can either induce or repress Bcl-6 expressionAna 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... - Chronic myeloid leukemia--advances in biology and new approaches to treatmentJohn M Goldman
Department of Haematology, Faculty of Medicine, Hammersmith Hospital, Imperial College London, London, United Kingdom
N Engl J Med 349:1451-64. 2003 - Dose-dependent effects of Bcr-Abl in cell line models of different stages of chronic myeloid leukemiaDavid 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... - 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-1Chikashi Yoshida
Department of Haematology, Imperial College London, Hammersmith Hospital, UK
Blood 109:1211-9. 2007.... - Management of chronic myeloid leukemia: targets for molecular therapyDavid 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... - Response to imatinib mesylate in patients with chronic myeloproliferative diseases with rearrangements of the platelet-derived growth factor receptor betaJane 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... - Allorestricted cytotoxic T cells specific for human CD45 show potent antileukemic activityPersis 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... - Overexpression of SOCS-2 in advanced stages of chronic myeloid leukemia: possible inadequacy of a negative feedback mechanismBeate 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... - Cytogenetic and molecular genetic aspects of chronic myeloid leukaemiaDavid 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... - Imatinib mesylate in combination with other chemotherapeutic drugs: in vitro studiesAlex 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... - Upregulation of the TGFbeta signalling pathway by Bcr-Abl: implications for haemopoietic cell growth and chronic myeloid leukaemiaGigi M O Møller
School of Biological Sciences, University of East Anglia, Norwich NR4 7TJ, UK
FEBS Lett 581:1329-34. 2007.... - Enhanced Bcr-Abl-specific antileukemic activity of arsenic trioxide (Trisenox) through glutathione-depletion in imatinib-resistant cellsHeiko 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... - Novel compounds with antiproliferative activity against imatinib-resistant cell linesEnrica 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... - Nuclear positioning of the BACH2 gene in BCR-ABL positive leukemic cellsAtsushi 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.... - The use of isobaric tag peptide labeling (iTRAQ) and mass spectrometry to examine rare, primitive hematopoietic cells from patients with chronic myeloid leukemiaStephen 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... - Mutations of the myeloid transcription factor CEBPA are not associated with the blast crisis of chronic myeloid leukaemiaThomas 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... - A novel K509I mutation of KIT identified in familial mastocytosis-in vitro and in vivo responsiveness to imatinib therapyLing 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... - Overcoming STI571 resistance with the farnesyl transferase inhibitor SCH66336Russell 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... - Acquired resistance to imatinib mesylate: selection for pre-existing mutant cellsLucio Luzzatto
Blood 100:1105. 2002 - Mutation in the ATP-binding site of BCR-ABL in a patient with chronic myeloid leukaemia with increasing resistance to STI571Christophe Barthe
, , 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... - Imatinib mesylate (STI-571) reduces Bcr-Abl-mediated vascular endothelial growth factor secretion in chronic myelogenous leukemiaJohn 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... - Imatinib: can one outwit chronic myeloid leukemia?Lucio Luzzatto
Haematologica 87:898-901. 2002 - MDR1 gene overexpression confers resistance to imatinib mesylate in leukemia cell line modelsFrancois 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... - Cross-resistance of imatinib mesylate and 17-AAG in imatinib-resistant cells that overexpress BCR-ABLJulian Topaly
Br J Haematol 121:672-3. 2003 - Bcr-Abl kinase modulates the translation regulators ribosomal protein S6 and 4E-BP1 in chronic myelogenous leukemia cells via the mammalian target of rapamycinChi 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... - Comparative gene expression profile of p185(Bcr-Abl) versus p210(Bcr-Abl) expressing cellsAlex J Tipping
Leuk Res 28:219-20. 2004 - Overproduction of BCR-ABL induces apoptosis in imatinib mesylate-resistant cell linesVanessa Desplat
, , Bordeaux Cedex, France
Cancer 103:102-10. 2005..CONCLUSIONS: Thus, imatinib removal led to apoptosis of BCR-ABL-overexpressing leukemic cells, a phenomenon that could be exploited to sensitize imatinib-resistant cells to the cytotoxic effect of other drugs... - Analysis of total phosphotyrosine levels in CD34+ cells from CML patients to predict the response to imatinib mesylate treatmentBeate Schultheis
Blood 105:4893-4. 2005 - Transient response to imatinib mesylate (STI571) in a patient with the ETV6-ABL t(9;12) translocationStephen 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... - Inactivation of HOXA genes by hypermethylation in myeloid and lymphoid malignancy is frequent and associated with poor prognosisGordon 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... - Production of P-glycoprotein from the MDR1 upstream promoter is insufficient to affect the response to first-line chemotherapy in advanced breast cancerSelina 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....