Erosion of the chronic myeloid leukaemia stem cell pool by PPARγ agonists

[1]  J. Qi,et al.  Targeting STAT5 in Hematologic Malignancies through Inhibition of the Bromodomain and Extra-Terminal (BET) Bromodomain Protein BRD2 , 2014, Molecular Cancer Therapeutics.

[2]  Yu-Chung Yang,et al.  Cited2 in hematopoietic stem cell function , 2013, Current opinion in hematology.

[3]  J. Cayuela,et al.  Targeting STAT5 Expression Resulted in Molecular Response Improvement in Patients with Chronic Phase CML Treated with Imatinib , 2012 .

[4]  R. Clark,et al.  Peroxisome proliferator-activated receptor activation increases imatinib uptake and killing of chronic myeloid leukemia cells. , 2012, Experimental hematology.

[5]  P. Pandolfi,et al.  A PML–PPAR-δ pathway for fatty acid oxidation regulates hematopoietic stem cell maintenance , 2012, Nature Medicine.

[6]  S. Dunwoodie,et al.  HIF-1α deletion partially rescues defects of hematopoietic stem cell quiescence caused by Cited2 deficiency. , 2012, Blood.

[7]  R. Bhatia,et al.  Activation of stress response gene SIRT1 by BCR-ABL promotes leukemogenesis. , 2012, Blood.

[8]  Peter Dirks,et al.  Cancer stem cells: an evolving concept , 2012, Nature Reviews Cancer.

[9]  F. Aguilo,et al.  Quantitative trait mapping reveals a regulatory axis involving peroxisome proliferator-activated receptors, PRDM16, transforming growth factor-β2 and FLT3 in hematopoiesis. , 2011, Blood.

[10]  A. Turhan,et al.  Chronic myeloid leukemia stem cells in the era of targeted therapies: resistance, persistence and long-term dormancy , 2011, Oncotarget.

[11]  E. Vellenga,et al.  Identification of HIF2alpha as an important STAT5 target gene in human hematopoietic stem cells. , 2011, Blood.

[12]  B. Druker,et al.  Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity. , 2011, The Journal of clinical investigation.

[13]  S. Koschmieder,et al.  Mouse models as tools to understand and study BCR-ABL1 diseases. , 2011, American journal of blood research.

[14]  D. Carson,et al.  Repression of beta-catenin signaling by PPAR gamma ligands. , 2010, European journal of pharmacology.

[15]  L. Hennighausen,et al.  Stat5 is indispensable for the maintenance of bcr/abl-positive leukaemia , 2010, EMBO molecular medicine.

[16]  P. Devillier,et al.  Imatinib assay by HPLC with photodiode-array UV detection in plasma from patients with chronic myeloid leukemia: Comparison with LC-MS/MS. , 2010, Clinica chimica acta; international journal of clinical chemistry.

[17]  T. Chou.  Drug combination studies and their synergy quantification using the Chou-Talalay method. , 2010, Cancer research.

[18]  C. Peng,et al.  Loss of the Alox5 gene impairs leukemia stem cells and prevents chronic myeloid leukemia , 2009, Nature Genetics.

[19]  M. Koutsilieris,et al.  IL-6 and PPARγ Signalling in Human PC-3 Prostate Cancer Cells , 2009 .

[20]  J. Klawitter,et al.  Abnormalities in Glucose Uptake and Metabolism in Imatinib-Resistant Human BCR-ABL–Positive Cells , 2009, Clinical Cancer Research.

[21]  W. Tse,et al.  Conditional deletion of STAT5 in adult mouse hematopoietic stem cells causes loss of quiescence and permits efficient nonablative stem cell replacement. , 2009, Blood.

[22]  T. Harkness,et al.  Troglitazone reverses the multiple drug resistance phenotype in cancer cells , 2009, Drug design, development and therapy.

[23]  Ji Luo,et al.  Principles of Cancer Therapy: Oncogene and Non-oncogene Addiction , 2009, Cell.

[24]  Jaspal Kaeda,et al.  Imatinib for newly diagnosed patients with chronic myeloid leukemia: incidence of sustained responses in an intention-to-treat analysis. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[25]  N. Déglon,et al.  Human and simian immunodeficiency viruses deregulate early hematopoiesis through a Nef/PPARgamma/STAT5 signaling pathway in macaques. , 2008, The Journal of clinical investigation.

[26]  M. Simon,et al.  The N-Terminal Transactivation Domain Confers Target Gene Specificity of Hypoxia-inducible Factors HIF-1α and HIF-2α , 2007 .

[27]  Yu-Chung Yang,et al.  Cited2 is required for normal hematopoiesis in the murine fetal liver. , 2007, Blood.

[28]  Y. Miyazaki,et al.  Reduction in Hematocrit and Hemoglobin Following Pioglitazone Treatment is not Hemodilutional in Type II Diabetes Mellitus , 2007, Clinical pharmacology and therapeutics.

[29]  T. Holyoake,et al.  Nilotinib exerts equipotent antiproliferative effects to imatinib and does not induce apoptosis in CD34+ CML cells. , 2007, Blood.

[30]  M. Copland,et al.  Dasatinib (BMS-354825) targets an earlier progenitor population than imatinib in primary CML but does not eliminate the quiescent fraction. , 2006, Blood.

[31]  A. Szántó,et al.  Retinoids Potentiate Peroxisome Proliferator-Activated Receptor γ Action in Differentiation, Gene Expression, and Lipid Metabolic Processes in Developing Myeloid Cells , 2005, Molecular Pharmacology.

[32]  H. Cavé,et al.  Standardization and quality control studies of ‘real-time’ quantitative reverse transcriptase polymerase chain reaction of fusion gene transcripts for residual disease detection in leukemia – A Europe Against Cancer Program , 2003, Leukemia.

[33]  T. Holyoake,et al.  Primitive, quiescent, Philadelphia-positive stem cells from patients with chronic myeloid leukemia are insensitive to STI571 in vitro. , 2002, Blood.

[34]  P. Vidalain,et al.  Characterization of novel safe lentiviral vectors derived from simian immunodeficiency virus (SIVmac251) that efficiently transduce mature human dendritic cells , 2000, Gene Therapy.

[35]  J. Marine,et al.  Antiapoptotic activity of Stat5 required during terminal stages of myeloid differentiation. , 2000, Genes & development.

[36]  A. Yoshimura,et al.  CIS, a cytokine inducible SH2 protein, is a target of the JAK-STAT5 pathway and modulates STAT5 activation. , 1997, Blood.