Loss of P-glycoprotein expression in hematopoietic stem cells does not improve responses to imatinib in a murine model of chronic myelogenous leukemia

[1]  J. Schellens,et al.  The effect of Bcrp1 (Abcg2) on the in vivo pharmacokinetics and brain penetration of imatinib mesylate (Gleevec): implications for the use of breast cancer resistance protein and P-glycoprotein inhibitors to enable the brain penetration of imatinib in patients. , 2005, Cancer research.

[2]  R. Ren,et al.  Mechanisms of BCR–ABL in the pathogenesis of chronic myelogenous leukaemia , 2005, Nature Reviews Cancer.

[3]  Mariël Brok,et al.  Imatinib mesylate (STI571) is a substrate for the breast cancer resistance protein (BCRP)/ABCG2 drug pump. , 2004, Blood.

[4]  P. Houghton,et al.  Imatinib Mesylate Is a Potent Inhibitor of the ABCG2 (BCRP) Transporter and Reverses Resistance to Topotecan and SN-38 in Vitro , 2004, Cancer Research.

[5]  G. Ehninger,et al.  P-glycoprotein-mediated drug efflux is a resistance mechanism of chronic myelogenous leukemia cells to treatment with imatinib mesylate , 2004, Leukemia.

[6]  L. Ashman,et al.  Overexpression of P-glycoprotein in K562 cells does not confer resistance to the growth inhibitory effects of imatinib (STI571) in vitro. , 2003, Blood.

[7]  Michael F. Clarke,et al.  Applying the principles of stem-cell biology to cancer , 2003, Nature Reviews Cancer.

[8]  T. Lu,et al.  Hematopoietic cells from mice that are deficient in both Bcrp1/Abcg2 and Mdr1a/1b develop normally but are sensitized to mitoxantrone. , 2003, BioTechniques.

[9]  J. Melo,et al.  Chronic myeloid leukemia--advances in biology and new approaches to treatment. , 2003, The New England journal of medicine.

[10]  H. Mizoguchi,et al.  Anti-proliferative effect of the abl tyrosine kinase inhibitor STI571 on the P-glycoprotein positive K562/ADM cell line. , 2003, Cancer Letters.

[11]  T. Furukawa,et al.  Reversal of the resistance to STI571 in human chronic myelogenous leukemia K562 cells , 2003, Cancer science.

[12]  G. Daley,et al.  Mechanisms of Autoinhibition and STI-571/Imatinib Resistance Revealed by Mutagenesis of BCR-ABL , 2003, Cell.

[13]  J. Melo,et al.  MDR1 gene overexpression confers resistance to imatinib mesylate in leukemia cell line models. , 2003, Blood.

[14]  Francisco Cervantes,et al.  Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia. , 2003, The New England journal of medicine.

[15]  W. Elmquist,et al.  Distribution of STI-571 to the Brain Is Limited by P-Glycoprotein-Mediated Efflux , 2003, Journal of Pharmacology and Experimental Therapeutics.

[16]  M. Zucchetti,et al.  α1 Acid Glycoprotein Binds to Imatinib (STI571) and Substantially Alters Its Pharmacokinetics in Chronic Myeloid Leukemia Patients , 2003 .

[17]  T. Furukawa,et al.  Reversal of P-glycoprotein mediated multidrug resistance by a newly synthesized 1,4-benzothiazipine derivative, JTV-519. , 2002, Cancer letters.

[18]  G. Sauvageau,et al.  Oncogenic interaction between BCR-ABL and NUP98-HOXA9 demonstrated by the use of an in vitro purging culture system. , 2002, Blood.

[19]  J. Schuetz,et al.  Bcrp1 gene expression is required for normal numbers of side population stem cells in mice, and confers relative protection to mitoxantrone in hematopoietic cells in vivo , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[20]  J. Kuriyan,et al.  Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia. , 2002, Cancer cell.

[21]  G. Kéri,et al.  Interaction of tyrosine kinase inhibitors with the human multidrug transporter proteins, MDR1 and MRP1. , 2002, Biochimica et biophysica acta.

[22]  R. Larson,et al.  Imatinib induces hematologic and cytogenetic responses in patients with chronic myelogenous leukemia in myeloid blast crisis: results of a phase II study. , 2002, Blood.

[23]  M. Baccarani,et al.  Imatinib induces durable hematologic and cytogenetic responses in patients with accelerated phase chronic myeloid leukemia: results of a phase 2 study. , 2002, Blood.

[24]  R. Ilaria,et al.  Establishment of a murine model for therapy-treated chronic myelogenous leukemia using the tyrosine kinase inhibitor STI571. , 2001, Blood.

[25]  H. Nakauchi,et al.  The ABC transporter Bcrp1/ABCG2 is expressed in a wide variety of stem cells and is a molecular determinant of the side-population phenotype , 2001, Nature Medicine.

[26]  P. N. Rao,et al.  Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification , 2001, Science.

[27]  C. Sawyers,et al.  Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. , 2001, The New England journal of medicine.

[28]  T. Lu,et al.  Enforced P-glycoprotein pump function in murine bone marrow cells results in expansion of side population stem cells in vitro and repopulating cells in vivo. , 2000, Blood.

[29]  J. Melo,et al.  Selection and characterization of BCR-ABL positive cell lines with differential sensitivity to the tyrosine kinase inhibitor STI571: diverse mechanisms of resistance. , 2000, Blood.

[30]  George Q. Daley,et al.  The P190, P210, and P230 Forms of the BCR/ABL Oncogene Induce a Similar Chronic Myeloid Leukemia–like Syndrome in Mice but Have Different Lymphoid Leukemogenic Activity , 1999, The Journal of experimental medicine.

[31]  X Zhang,et al.  Bcr-Abl efficiently induces a myeloproliferative disease and production of excess interleukin-3 and granulocyte-macrophage colony-stimulating factor in mice: a novel model for chronic myelogenous leukemia. , 1998, Blood.

[32]  Jon C. Aster,et al.  Efficient and Rapid Induction of a Chronic Myelogenous Leukemia-Like Myeloproliferative Disease in Mice Receiving P210 bcr/abl-Transduced Bone Marrow , 1998 .

[33]  B. Sorrentino,et al.  Transduction of murine bone marrow cells with an MDR1 vector enables ex vivo stem cell expansion, but these expanded grafts cause a myeloproliferative syndrome in transplanted mice. , 1998, Blood.

[34]  A. Nienhuis,et al.  An improved method for generating retroviral producer clones for vectors lacking a selectable marker gene. , 1998, Blood cells, molecules & diseases.

[35]  P. Borst,et al.  Normal viability and altered pharmacokinetics in mice lacking mdr1-type (drug-transporting) P-glycoproteins. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[36]  K. McDonagh,et al.  Expression of retroviral vectors containing the human multidrug resistance 1 cDNA in hematopoietic cells of transplanted mice. , 1995, Blood.

[37]  I. Roninson,et al.  Expression and activity of P-glycoprotein, a multidrug efflux pump, in human hematopoietic stem cells , 1991, Cell.

[38]  Mariël Brok,et al.  Imatinib mesylate ( STI 571 ) is a substrate for the breast cancer resistance protein ( BCRP ) / ABCG 2 drug pump , 2004 .

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