Francois Xavier Mahon

Summary

Country: France

Publications

  1. ncbi 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
  2. ncbi JAK the trigger
    Francois Xavier Mahon
    Laboratoire d hématopoïèse leucémique et cible thérapeutique, Universite Victor Segalen Bordeaux 2, INSERM E0217, 33076 Bordeaux Cedex, France
    Oncogene 24:7125-6. 2005
  3. ncbi [Leucemogenesis of chronic myelogenous leukemia]
    Francois Xavier Mahon
    Laboratoire d Hematologie, CHU de Bordeaux, INSERM E0217, Universite Victor Segalen Bordeaux 2, 33076 Bordeaux Cedex
    Rev Prat 55:1642-6. 2005
  4. ncbi [Chronic myeloid leukemia and tyrosine kinase inhibitors]
    F X Mahon
    Laboratoire de Greffe de Moelle, Universite Victor Segalen, UMR CNRS 5540, 146, rue Leo Saignat, 33076 Bordeaux, France
    Rev Med Interne 22:894-9. 2001
  5. ncbi Pharmacologic monitoring and determinants of intracytoplasmic drug levels
    Francois Xavier Mahon
    Laboratoire Hématopoïèse Leucémique et Cible Thérapeutique, Inserm U876, Universite Victor Segalen Bordeaux 2, 146, rue Leo Saignat 33076, Bordeaux Cedex, France
    Best Pract Res Clin Haematol 22:381-6. 2009
  6. doi Discontinuation of imatinib in patients with chronic myeloid leukaemia who have maintained complete molecular remission for at least 2 years: the prospective, multicentre Stop Imatinib (STIM) trial
    Francois Xavier Mahon
    Laboratoire d Hématologie et Service des Maladies du Sang, Centre Hospitalier Universitaire de Bordeaux, Bordeaux, France
    Lancet Oncol 11:1029-35. 2010
  7. ncbi Rapid detection of phosphotyrosine proteins by flow cytometric analysis in Bcr-Abl-positive cells
    Vanessa Desplat
    Laboratoire Hématopoïèse Normale et Pathologique, FRE CNRS 2617, Universite Victor Segalen, rue Leo Saignat, 33076 Bordeaux Cedex, France
    Cytometry A 62:35-45. 2004
  8. ncbi ABT-737 increases tyrosine kinase inhibitor-induced apoptosis in chronic myeloid leukemia cells through XIAP downregulation and sensitizes CD34(+) CD38(-) population to imatinib
    Kelly Airiau
    Laboratoire d Hématopoïèse Leucémique et Cibles Thérapeutiques, INSERM 1035, Université Bordeaux Segalen, Bordeaux Cedex, France
    Exp Hematol 40:367-78.e2. 2012
  9. ncbi 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
  10. pmc A single nucleotide polymorphism in cBIM is associated with a slower achievement of major molecular response in chronic myeloid leukaemia treated with imatinib
    Vanessa Augis
    Université Bordeaux Segalen and INSERM U1035 Bordeaux, Bordeaux, France Laboratoire d hématologie, Centre Hospitalier Universitaire de Bordeaux, Bordeaux, France
    PLoS ONE 8:e78582. 2013

Detail Information

Publications49

  1. ncbi 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...
  2. ncbi JAK the trigger
    Francois Xavier Mahon
    Laboratoire d hématopoïèse leucémique et cible thérapeutique, Universite Victor Segalen Bordeaux 2, INSERM E0217, 33076 Bordeaux Cedex, France
    Oncogene 24:7125-6. 2005
    ....
  3. ncbi [Leucemogenesis of chronic myelogenous leukemia]
    Francois Xavier Mahon
    Laboratoire d Hematologie, CHU de Bordeaux, INSERM E0217, Universite Victor Segalen Bordeaux 2, 33076 Bordeaux Cedex
    Rev Prat 55:1642-6. 2005
    ..These new specific drugs and their effects on the chronic myelogenous leukemia must be taken into account to explain the physiopathology of the disease...
  4. ncbi [Chronic myeloid leukemia and tyrosine kinase inhibitors]
    F X Mahon
    Laboratoire de Greffe de Moelle, Universite Victor Segalen, UMR CNRS 5540, 146, rue Leo Saignat, 33076 Bordeaux, France
    Rev Med Interne 22:894-9. 2001
    ....
  5. ncbi Pharmacologic monitoring and determinants of intracytoplasmic drug levels
    Francois Xavier Mahon
    Laboratoire Hématopoïèse Leucémique et Cible Thérapeutique, Inserm U876, Universite Victor Segalen Bordeaux 2, 146, rue Leo Saignat 33076, Bordeaux Cedex, France
    Best Pract Res Clin Haematol 22:381-6. 2009
    ....
  6. doi Discontinuation of imatinib in patients with chronic myeloid leukaemia who have maintained complete molecular remission for at least 2 years: the prospective, multicentre Stop Imatinib (STIM) trial
    Francois Xavier Mahon
    Laboratoire d Hématologie et Service des Maladies du Sang, Centre Hospitalier Universitaire de Bordeaux, Bordeaux, France
    Lancet Oncol 11:1029-35. 2010
    ..We aimed to assess whether imatinib can be discontinued without occurrence of molecular relapse in patients in complete molecular remission (CMR) while on imatinib...
  7. ncbi Rapid detection of phosphotyrosine proteins by flow cytometric analysis in Bcr-Abl-positive cells
    Vanessa Desplat
    Laboratoire Hématopoïèse Normale et Pathologique, FRE CNRS 2617, Universite Victor Segalen, rue Leo Saignat, 33076 Bordeaux Cedex, France
    Cytometry A 62:35-45. 2004
    ..In this study, we developed a method to detect the phosphotyrosine proteins by flow cytometry and we asked whether phosphorylation was affected by imatinib mesylate treatment...
  8. ncbi ABT-737 increases tyrosine kinase inhibitor-induced apoptosis in chronic myeloid leukemia cells through XIAP downregulation and sensitizes CD34(+) CD38(-) population to imatinib
    Kelly Airiau
    Laboratoire d Hématopoïèse Leucémique et Cibles Thérapeutiques, INSERM 1035, Université Bordeaux Segalen, Bordeaux Cedex, France
    Exp Hematol 40:367-78.e2. 2012
    ..Interestingly, a lethal effect was also observed in the more immature CD34(+)CD38(-) TKI-insensitive population. Combination therapy might by an interesting strategy for the treatment of CML patients...
  9. ncbi 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...
  10. pmc A single nucleotide polymorphism in cBIM is associated with a slower achievement of major molecular response in chronic myeloid leukaemia treated with imatinib
    Vanessa Augis
    Université Bordeaux Segalen and INSERM U1035 Bordeaux, Bordeaux, France Laboratoire d hématologie, Centre Hospitalier Universitaire de Bordeaux, Bordeaux, France
    PLoS ONE 8:e78582. 2013
    ..The present study aimed at identifying mutations in the BIM sequence that could lead to imatinib resistance independently of BCR-ABL mutations...
  11. ncbi Imatinib and nilotinib induce apoptosis of chronic myeloid leukemia cells through a Bim-dependant pathway modulated by cytokines
    Francis Belloc
    Laboratoire d Hematologie, Hopital du Haut leveque, Pessac, France
    Cancer Biol Ther 6:912-9. 2007
    ..Thus BCR-ABL inhibition restores the cytokine dependence but is not sufficient to induce apoptosis when other signaling pathways are activated...
  12. ncbi Therapeutic drug monitoring of imatinib in chronic myeloid leukemia: experience from 1216 patients at a centralized laboratory
    Stephane Bouchet
    Univ Bordeaux, F 33000, Bordeaux, France INSERM U657, F 33000, Bordeaux, France CHU Bordeaux, F 33000, Bordeaux, France
    Fundam Clin Pharmacol 27:690-7. 2013
    ..69 and 2.08, respectively. These data support in real-life setting that imatinib C(min) threshold of 1000 ng/mL is associated with major and complete molecular response and that TDM could play an important role in dose optimization...
  13. ncbi Multidrug resistance gene (MDR1) polymorphisms are associated with major molecular responses to standard-dose imatinib in chronic myeloid leukemia
    Stéphanie Dulucq
    Laboratoire Hématopoïèse Leucémique et Cible Thérapeutique, Universite Victor Segalen Bordeaux 2, Inserm U876, Bordeaux, France
    Blood 112:2024-7. 2008
    ..6%; P = .021). Hence, we demonstrated the usefulness of these single nucleotide polymorphisms in the identification of CML who may or may not respond optimally to imatinib...
  14. ncbi Quantification of imatinib in human plasma by high-performance liquid chromatography-tandem mass spectrometry
    Karine Titier
    Department of Clinical Pharmacology and Toxicology, Pellegrin Hospital and University Victor Segalen, 33076 Bordeaux, France
    Ther Drug Monit 27:634-40. 2005
    ..It can be used to evaluate patient adherence to daily oral therapy, drug-drug interactions, or pharmacokinetic/pharmacodynamic relationships...
  15. ncbi 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...
  16. ncbi Evidence that resistance to nilotinib may be due to BCR-ABL, Pgp, or Src kinase overexpression
    Francois Xavier Mahon
    Hématopoïèse Leucémique et Cible Thérapeutique, Inserm U876, Universite Victor Segalen, Laboratoire d hématologie CHU de Bordeaux, Bordeaux Cedex, France
    Cancer Res 68:9809-16. 2008
    ..Such mechanisms of resistance are close to those observed in imatinib-resistant cell lines and emphasize the critical role of Lyn in nilotinib resistance...
  17. doi Quantitative phosphoproteomics revealed interplay between Syk and Lyn in the resistance to nilotinib in chronic myeloid leukemia cells
    Romain Gioia
    Hématopoïèse Leucémique et Cible Thérapeutique, Inserm U1035, Universite Victor Segalen, Bordeaux, France
    Blood 118:2211-21. 2011
    ..We conclude that an oncogenic signaling mediated by Lyn and Syk can bypass the need of Bcr-Abl in CML cells. Thus, targeting these kinases may be of therapeutic value to override imatinib or nilotinib resistance in CML...
  18. ncbi Proteomic analysis of an imatinib-resistant K562 cell line highlights opposing roles of heat shock cognate 70 and heat shock 70 proteins in resistance
    Marion Pocaly
    U876 INSERM, Universite Victor Segalen Bordeaux 2, Hématopoïèse Leucémique et Cibles Thérapeutiques, Bordeaux, France
    Proteomics 8:2394-406. 2008
    ..In contrast, the induced decreased expression of Hsc70 was accompanied by a greater overexpression of Hsp70. This proteomic study therefore suggests opposing roles of Hsp70 and Hsc70 in imatinib resistance...
  19. ncbi A SIN lentiviral vector containing PIGA cDNA allows long-term phenotypic correction of CD34+-derived cells from patients with paroxysmal nocturnal hemoglobinuria
    David Robert
    INSERM E 0217, Laboratoire de Pathologie Moléculaire et Thérapie Génique, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat, 33076 Bordeaux, France
    Mol Ther 7:304-16. 2003
    ..This expression was stable during erythroid, myeloid, and megakaryocytic liquid culture differentiation. CD59 surface cell expression was fully restored during 5 weeks of long-term culture...
  20. ncbi Molecular remission in chronic myeloid leukemia patients with sustained complete cytogenetic remission after imatinib mesylate treatment
    Marie Colombat
    Laboratoire d hématologie Université Victor Segalen, Bordeaux, France
    Haematologica 91:162-8. 2006
    ..However, the ultimate goal of therapy for CML is complete elimination of Philadelphia chromosome positive cells or BCR-ABL rearrangements. We studied molecular responses in CML patients in CCR after imatinib treatment...
  21. doi Imatinib plus peginterferon alfa-2a in chronic myeloid leukemia
    Claude Preudhomme
    Laboratoire d Hematologie, Centre Hospitalier Universitaire de Lille, and INSERM Unité 837, Lille, France
    N Engl J Med 363:2511-21. 2010
    ..However, only a minority of patients treated with imatinib have a complete molecular remission...
  22. pmc Phosphorylation of serine palmitoyltransferase long chain-1 (SPTLC1) on tyrosine 164 inhibits its activity and promotes cell survival
    Said Taouji
    Inserm U1053, 33076 Bordeaux, France
    J Biol Chem 288:17190-201. 2013
    ..Our observations provide a mechanistic explanation for imatinib-mediated cell death and a novel avenue for therapeutic strategies...
  23. ncbi Hypoxia modifies proliferation and differentiation of CD34(+) CML cells
    Vanessa Desplat
    Laboratoire de Greffe de Moelle, Universite Bordeaux 2, Bordeaux, France
    Stem Cells 20:347-54. 2002
    ..These effects could be linked to inhibition by hypoxia of the tyrosine hyperphosphorylation of cellular proteins, a major hallmark of CML cells...
  24. ncbi [Leukemogenesis and new therapy development: the example of chronic myelogenous leukemia]
    G Etienne
    Laboratoire de Greffe de Moelle, , 146, , 33076 Bordeaux, France
    Bull Cancer 88:651-8. 2001
    ..STI571 is an original therapeutic approach which may be used as a model for the development of other drugs in cancer...
  25. doi Is going for cure in chronic myeloid leukemia possible and justifiable?
    Francois Xavier Mahon
    Laboratoire d Hematologie, Centre Hospitalier Universitaire de Bordeaux, Bordeaux Cedex, France
    Hematology Am Soc Hematol Educ Program 2012:122-8. 2012
    ..If we win this battle, this progress will certainly benefit the treatment and management of other leukemias and solid tumors and will validate this new topic...
  26. pmc Mycophenolic Acid overcomes imatinib and nilotinib resistance of chronic myeloid leukemia cells by apoptosis or a senescent-like cell cycle arrest
    Claire Drullion
    Laboratoire Hématopoïèse Leucémique et Cibles Thérapeutiques, Inserm U1035, Université Bordeaux Segalen, 146 Rue Léo Saignat Bat TP 4e étage, 33076 Bordeaux, France
    Leuk Res Treatment 2012:861301. 2012
    ..These results show that MPA is an interesting tool to overcome resistance in vitro and in vivo mainly in the evolved phase of the disease...
  27. ncbi A method to measure deferasirox in plasma using HPLC coupled with MS/MS detection and its potential application
    Emmanuelle Chauzit
    Département de Pharmacologie Clinique et Toxicologie, CHU de Bordeaux, Bordeaux, France
    Ther Drug Monit 32:476-81. 2010
    ..It allows evaluation of patient compliance, drug-drug interactions, and further investigations of pharmacokinetic/pharmacodynamic relationships...
  28. ncbi Trough imatinib plasma levels are associated with both cytogenetic and molecular responses to standard-dose imatinib in chronic myeloid leukemia
    Stephane Picard
    Department of Clinical Pharmacology and Toxicology, Centre Hospitalier Universitaire de Bordeaux, Bordeaux, France
    Blood 109:3496-9. 2007
    ..Therefore, monitoring of imatinib plasma levels could be very useful for the management of patients with CML or should at least be checked in the case of treatment failure or suboptimal response...
  29. doi Triptolide cooperates with chemotherapy to induce apoptosis in acute myeloid leukemia cells
    Arnaud Pigneux
    CHU Bordeaux, Hopital Haut Leveque, Laboratoire d Hematologie, Pessac, France
    Exp Hematol 36:1648-59. 2008
    ..Triptolide has shown antitumor activity in a broad range of solid tumors and on leukemic cells in vitro...
  30. ncbi Expression of Flt3-ligand by the endothelial cell
    A Solanilla
    Laboratoire de Greffe de Moelle, Universite Victor Segalen, Bordeaux, France
    Leukemia 14:153-62. 2000
    ..This stimulation is essential to explain their modulatory effect on the generation of clonogenic cells in cocultures EC/hematopoietic progenitors. Leukemia (2000) 14, 153-162...
  31. pmc Variable behavior of iPSCs derived from CML patients for response to TKI and hematopoietic differentiation
    Aurélie Bedel
    Inserm U1035, Biothérapies des maladies génétiques et cancers, Bordeaux, France Université Bordeaux Segalen, Bordeaux, France
    PLoS ONE 8:e71596. 2013
    ..Thus, several clones of CML-iPSCs are a powerful model to decipher all the mechanisms leading to LSC survival following TKI therapy and are a promising tool for testing new therapeutic agents...
  32. doi Potent graft-versus-leukemia effect after reduced-intensity allogeneic SCT for intermediate-risk AML with FLT3-ITD or wild-type NPM1 and CEBPA without FLT3-ITD
    Gaëlle Labouré
    Service d Hématologie et de Thérapie Cellulaire, CHU Haut Levêque, Bordeaux, France
    Biol Blood Marrow Transplant 18:1845-50. 2012
    ..32; P = .01). A landmark analysis performed at day 185 after CR1 confirmed a lower CIR after allo. RIC-allo reduces the risk of relapse, suggesting a potent graft-versus-leukemia (GVL) effect in these patients at a high risk of relapse...
  33. pmc Expression of neurotrophins and their receptors in human bone marrow
    E Labouyrie
    Laboratoire d Histologie Embryologie, Universite Victor Segalen, Bordeaux, France
    Am J Pathol 154:405-15. 1999
    ..The local expression of neurotrophin genes suggests a wide range of paracrine and/or autocrine mode of action through their corresponding receptors within the bone marrow...
  34. ncbi Increased liposome-mediated gene transfer into haematopoietic cells grown in adhesion to stromal or fibroblast cell line monolayers
    G Marit
    Laboratoire de Greffe de Moelle, UMR CNRS 5540, Universite Victor Segalen Bordeaux 2, France
    Eur J Haematol 64:22-31. 2000
    ..30%) for the cell lines and 13.6% (range 8.2-24.2%) for CD34+ HPC. These results indicate that liposome-mediated transfection of HC is significantly increased when cells are grown in adherence to stroma or fibroblast monolayers...
  35. ncbi Differential effect of interferon alpha on chronic myelogenous leukaemia and normal haematopoietic progenitors in a stromal cell co-culture context: role of the flt3 ligand
    A Solanilla
    FR 60, Biologie des Greffes, Universite de Bordeaux 2, France
    Br J Haematol 109:382-7. 2000
    ....
  36. ncbi Ex vivo cytokine expansion of peripheral blood Ph-negative cells in chronic myeloid leukaemia
    F X Mahon
    Laboratoire de Greffe de Moelle, UMR CNRS 5540, FR60, Universite Victor Segalen Bordeaux 2, France
    Leuk Lymphoma 32:151-7. 1998
    ..Therefore ex vivo expansion of putatively normal hematopoietic progenitor cells from cytapheresis is feasible in CML...
  37. ncbi The impact of the combination of baseline risk group and cytogenetic response on the survival of patients with chronic myeloid leukemia treated with interferon alpha
    Joerg Hasford
    Universite Victor Segalen, Bordeaux, France University Hospital Groningen, Groningen, The Netherlands
    Haematologica 90:335-40. 2005
    ..MCR was defined as a reduction of Philadelphia chromosome-positive bone marrow cells to <or= 35%. The New CML score discriminated three risk groups with significantly different survival probabilities...
  38. pmc The necrotic signal induced by mycophenolic acid overcomes apoptosis-resistance in tumor cells
    Gwendaline Guidicelli
    CNRS UMR 5164, Bordeaux, France
    PLoS ONE 4:e5493. 2009
    ..The anti-viral agent ribavirin and the immunosuppressant mycophenolic acid (MPA) are potent inhibitors of IMPDH. We recently showed that IMPDH inhibition led to a necrotic signal requiring the activation of Cdc42...
  39. doi The stem cell factor-c-KIT pathway must be inhibited to enable apoptosis induced by BCR-ABL inhibitors in chronic myelogenous leukemia cells
    F Belloc
    Laboratoire d Hématopoïèse Leucémique et Cibles Thérapeutiques, Inserm U876, Universite Victor Segalen, Bordeaux Cedex, France
    Leukemia 23:679-85. 2009
    ..We conclude that the c-KIT pathway may substitute for BCR-ABL tyrosine kinase to activate survival signals, and that c-KIT must be inhibited besides Bcr-Abl to allow apoptosis of CML cells...
  40. ncbi The hematopoietic stem cell compartment of JAK2V617F-positive myeloproliferative disorders is a reflection of disease heterogeneity
    Chloe James
    INSERM, U876, Bordeaux, France
    Blood 112:2429-38. 2008
    ..These experiments provide new insights into the pathogenesis of JAK2V617F MPD and demonstrate that a JAK2 inhibitor needs to target the HSC compartment for optimal disease control in classical MPD...
  41. doi Bundles of Auer rods in blast cells and mature neutrophils in a non-promyelocytic acute myeloblastic leukaemia
    Estelle Guerin
    Laboratoire d Hématologie du CHU de Bordeaux, Bordeaux, France
    Br J Haematol 141:749. 2008
  42. doi Imatinib sensitizes T-cell lymphocytes from chronic myeloid leukemia patients to FasL-induced cell death: a brief communication
    Laurence Legros
    CNRS, Institute of Developmental Biology and Cancer Research Université de Nice, France
    J Immunother 35:154-8. 2012
    ....
  43. ncbi Follow-up of complete cytogenetic remission in patients with chronic myeloid leukemia after cessation of interferon alfa
    F X Mahon
    Service des Maladies du Sang, Centre Hospitalier Universitaire de Bordeaux, Bordeaux 2, France
    J Clin Oncol 20:214-20. 2002
    ..In this population of patients, the question of whether treatment should then be withdrawn is not yet resolved...
  44. doi The effect of imatinib (Glivec) on scleroderma and normal dermal fibroblasts: a preclinical study
    A Soria
    Inserm U876, University Victor Segalen Bordeaux 2, Bordeaux, France
    Dermatology 216:109-17. 2008
    ..Moreover, increased levels of PDGF and stimulatory autoantibodies to PDGFR have been identified in the serum of scleroderma patients...
  45. doi Deep molecular response in chronic myeloid leukemia: the new goal of therapy?
    Francois Xavier Mahon
    Authors Affiliations Laboratoire d Hématologie, Centre Hospitalier Universitaire de Bordeaux and Laboratoire Hématopoïèse Leucémique et Cible Thérapeutique, Biothérapies des maladies génétiques et cancers, Inserm U1035, Université Bordeaux Ségalen and Centre Régional de Lutte Contre le Cancer de Bordeaux et du Sud Ouest, Institut Bergonie, Departement d Oncologie Medicale, Bordeaux, France
    Clin Cancer Res 20:310-22. 2014
    ....
  46. ncbi Expression of the cell cycle regulators p14(ARF) and p16(INK4a) in chronic myeloid leukemia
    Marie Cividin
    Laboratoire d Hematologie, CHU de Poitiers, France
    Leuk Res 30:1273-8. 2006
    ..Although protein expression did not consistently match mRNA levels, a role for the two cell cycle regulators in the IFN-alpha signaling pathway is suggested as well as a relation with the resistance to IFN-alpha or imatinib therapy...
  47. ncbi Derivative (7)t(7;8)(q34;q21). a new additional cytogenetic abnormality in acute promyelocytic leukemia
    Jean Philippe Vial
    Laboratoire d Hematologie, Centre Hospitalier et Universitaire de Bordeaux, Bordeaux, France
    Cancer Genet Cytogenet 140:78-81. 2003
    ..As the 7q and 8q breakpoints were similar in both cases, the involvement of these critical regions in the pathogenesis and outcome of APL disease has to be determined...
  48. ncbi Expression of interferon-alpha (IFN-alpha) receptor 2c at diagnosis is associated with cytogenetic response in IFN-alpha-treated chronic myeloid leukemia
    C Barthe
    , , 146, , 33076 Bordeaux Cedex, France
    Blood 97:3568-73. 2001
    ..0001). (Blood. 2001;97:3568-3573)..
  49. ncbi Overexpression of the heat-shock protein 70 is associated to imatinib resistance in chronic myeloid leukemia
    M Pocaly
    E0217 INSERM, Universite Victor Segalen Bordeaux 2, Hématopoïèse Leucémique et Cibles Thérapeutiques, Bordeaux Cedex, France
    Leukemia 21:93-101. 2007
    ..Moreover, the overexpression of Hsp70 detected in imatinib-resistant CML patients supports this mechanism and identifies potentially a marker and a therapeutic target of CML evolution...