Mechanisms of Resistance to Imatinib and Second-Generation Tyrosine Inhibitors in Chronic Myeloid Leukemia

No abstract is available for this paper.

• Publication year

  2009

• Venue

  Clinical Cancer Research

• Publication date

  2009-12-15

• Fields of study

  Medicine

• Identifiers
  DOI 10.1158/1078-0432.CCR-09-1068PMID 20008852
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Molecular biology of bcr-abl1-positive chronic myeloid leukemia.

  2009cited by this paper
• CORRECTION TO “CHARACTERIZATION OF DASATINIB AND ITS STRUCTURAL ANALOGS AS CYP3A4 MECHANISM-BASED INACTIVATORS AND THE PROPOSED BIOACTIVATION PATHWAYS”

  2009cited by this paper
• Mechanisms of primary and secondary resistance to imatinib in chronic myeloid leukemia.

  2009cited by this paper
• Impact of baseline BCR-ABL mutations on response to nilotinib in patients with chronic myeloid leukemia in chronic phase.

  2009cited by this paper
• P-glycoprotein and Breast Cancer Resistance Protein Influence Brain Distribution of Dasatinib

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• Inhibition of MDR1 does not sensitize primitive chronic myeloid leukemia CD34+ cells to imatinib.

  2009cited by this paper
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  2009cited by this paper
• Activity of bosutinib, dasatinib, and nilotinib against 18 imatinib-resistant BCR/ABL mutants.

  2009cited by this paper
• The use of nilotinib or dasatinib after failure to 2 prior tyrosine kinase inhibitors: long-term follow-up.

  2009cited by this paper
• Brain Accumulation of Dasatinib Is Restricted by P-Glycoprotein (ABCB1) and Breast Cancer Resistance Protein (ABCG2) and Can Be Enhanced by Elacridar Treatment

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• Six-year follow-up of patients receiving imatinib for the first-line treatment of chronic myeloid leukemia

  2009cited by this paper
• Philadelphia-positive patients who already harbor imatinib-resistant Bcr-Abl kinase domain mutations have a higher likelihood of developing additional mutations associated with resistance to second- or third-line tyrosine kinase inhibitors.

  2009cited by this paper
• Nilotinib (AMN107, Tasigna) reverses multidrug resistance by inhibiting the activity of the ABCB1/Pgp and ABCG2/BCRP/MXR transporters.

  2009cited by this paper
• Clinical Relevance of a Pharmacogenetic Approach Using Multiple Candidate Genes to Predict Response and Resistance to Imatinib Therapy in Chronic Myeloid Leukemia

  2009cited by this paper
• Predictors of primary imatinib resistance in chronic myelogenous leukemia are distinct from those in secondary imatinib resistance.

  2009cited by this paper
• Multidrug resistance gene (MDR1) polymorphisms are associated with major molecular responses to standard-dose imatinib in chronic myeloid leukemia.

  2008cited by this paper
• Metabolism and Disposition of Dasatinib after Oral Administration to Humans

  2008cited by this paper
• Dasatinib Cellular Uptake and Efflux in Chronic Myeloid Leukemia Cells: Therapeutic Implications

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  2008cited by this paper
• molecule Beyond the increasing complexity of the immunomodulatory HLA-G

  2008cited by this paper
• Interaction of Imatinib with Human Organic Ion Carriers

  2008cited by this paper
• In vivo kinetics of kinase domain mutations in CML patients treated with dasatinib after failing imatinib.

  2008cited by this paper
• Evidence that resistance to nilotinib may be due to BCR-ABL, Pgp, or Src kinase overexpression.

  2008cited by this paper
• European LeukemiaNet criteria for failure or suboptimal response reliably identify patients with CML in early chronic phase treated with imatinib whose eventual outcome is poor.

  2008cited by this paper
• Nilotinib: a second-generation tyrosine kinase inhibitor for the treatment of chronic myelogenous leukemia.

  2008cited by this paper
• CML Patients with Low OCT-1 Activity Achieve Better Molecular Responses on High Dose Imatinib Than on Standard Dose. Those with High OCT-1 Activity Have Excellent Responses on Either Dose: A TOPS Correlative Study

  2008cited by this paper
• BMS-214662 potently induces apoptosis of chronic myeloid leukemia stem and progenitor cells and synergizes with tyrosine kinase inhibitors.

  2008cited by this paper
• Effects of dasatinib on SRC kinase activity and downstream intracellular signaling in primitive chronic myelogenous leukemia hematopoietic cells.

  2008cited by this paper
• Preclinical pharmacokinetics and in vitro metabolism of dasatinib (BMS-354825): a potent oral multi-targeted kinase inhibitor against SRC and BCR-ABL

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• Sequential mutations causing resistance to both Imatinib Mesylate and Dasatinib in a chronic myeloid leukaemia patient progressing to lymphoid blast crisis.

  2008cited by this paper
• Imatinib pharmacokinetics and its correlation with response and safety in chronic-phase chronic myeloid leukemia: a subanalysis of the IRIS study.

  2008cited by this paper
• CXCR4 up-regulation by imatinib induces chronic myelogenous leukemia (CML) cell migration to bone marrow stroma and promotes survival of quiescent CML cells

  2008cited by this paper
• State-of-the-art in the treatment of chronic myeloid leukaemia

  2008cited by this paper
• Finding of kinase domain mutations in patients with chronic phase chronic myeloid leukemia responding to imatinib may identify those at high risk of disease progression.

  2008cited by this paper
• Imatinib mesylate and nilotinib (AMN107) exhibit high-affinity interaction with ABCG2 on primitive hematopoietic stem cells

  2007cited by this paper
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  2007cited by this paper
• Dynamics of BCR-ABL kinase domain mutations in chronic myeloid leukemia after sequential treatment with multiple tyrosine kinase inhibitors.

  2007cited by this paper
• Sequential ABL kinase inhibitor therapy selects for compound drug-resistant BCR-ABL mutations with altered oncogenic potency.

  2007cited by this paper
• Chronic myeloid leukemia stem cells possess multiple unique features of resistance to BCR-ABL targeted therapies

  2007cited by this paper
• Nilotinib exerts equipotent antiproliferative effects to imatinib and does not induce apoptosis in CD34+ CML cells.

  2007cited by this paper
• Growth factor stimulation reduces residual quiescent chronic myelogenous leukemia progenitors remaining after imatinib treatment.

  2007cited by this paper
• A Half-Log Increase in BCR-ABL RNA Predicts a Higher Risk of Relapse in Patients with Chronic Myeloid Leukemia with an Imatinib-Induced Complete Cytogenetic Response

  2007cited by this paper
• Clinical outcome of 27 imatinib mesylate-resistant chronic myelogenous leukemia patients harboring a T315I BCR-ABL mutation

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  2007cited by this paper
• Part I: mechanisms of resistance to imatinib in chronic myeloid leukaemia.

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• Most CML patients who have a suboptimal response to imatinib have low OCT-1 activity: higher doses of imatinib may overcome the negative impact of low OCT-1 activity.

  2007cited by this paper
• Phosphorylation of the ATP-binding loop directs oncogenicity of drug-resistant BCR-ABL mutants

  2006cited by this paper
• Targeting multiple kinase pathways in leukemic progenitors and stem cells is essential for improved treatment of Ph+ leukemia in mice

  2006cited by this paper
• OCT-1-mediated influx is a key determinant of the intracellular uptake of imatinib but not nilotinib (AMN107): reduced OCT-1 activity is the cause of low in vitro sensitivity to imatinib.

  2006cited by this paper
• The presence of a BCR-ABL mutant allele in CML does not always explain clinical resistance to imatinib

  2006cited by this paper
• Mutation status and clinical outcome of 89 imatinib mesylate-resistant chronic myelogenous leukemia patients: a retrospective analysis from the French intergroup of CML (Fi(ϕ)-LMC GROUP)

  2006cited by this paper
• Role of BCR/ABL gene-expression levels in determining the phenotype and imatinib sensitivity of transformed human hematopoietic cells.

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  2006cited by this paper
• Dasatinib (BMS-354825) targets an earlier progenitor population than imatinib in primary CML but does not eliminate the quiescent fraction.

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  2006cited by this paper
• Functional ABCG2 is overexpressed on primary CML CD34+ cells and is inhibited by imatinib mesylate.

  2006cited by this paper
• Contribution of ABL Kinase Domain Mutations to Imatinib Resistance in Different Subsets of Philadelphia-Positive Patients: By the GIMEMA Working Party on Chronic Myeloid Leukemia

  2006cited by this paper
• Kinase Domain Mutants of Bcr-Abl Exhibit Altered Transformation Potency, Kinase Activity, and Substrate Utilization, Irrespective of Sensitivity to Imatinib

  2006cited by this paper
• Quantitative molecular monitoring of BCR-ABL and MDR1 transcripts in patients with chronic myeloid leukemia during Imatinib treatment.

  2005cited by this paper
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  2005cited by this paper
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  2005cited by this paper
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• High-sensitivity detection of BCR-ABL kinase domain mutations in imatinib-naive patients: correlation with clonal cytogenetic evolution but not response to therapy.

  2005cited by this paper
• Bcr-Abl expression levels determine the rate of development of resistance to imatinib mesylate in chronic myeloid leukemia.

  2005cited by this paper
• Regulation of the c-Abl and Bcr–Abl tyrosine kinases

  2004cited by this paper
• Molecular interdiction of Src-family kinase signaling in hematopoietic cells

  2004cited by this paper
• Clonal evolution and lack of cytogenetic response are adverse prognostic factors for hematologic relapse of chronic phase CML patients treated with imatinib mesylate.

  2004cited by this paper
• Active transport of imatinib into and out of cells: implications for drug resistance.

  2004cited by this paper
• Novel single nucleotide polymorphisms of organic cation transporter 1 (SLC22A1) affecting transport functions.

  2004cited by this paper
• Overriding Imatinib Resistance with a Novel ABL Kinase Inhibitor

  2004cited by this paper
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  2004cited by this paper
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  2004cited by this paper
• A Bcr/Abl-independent, Lyn-dependent Form of Imatinib Mesylate (STI-571) Resistance Is Associated with Altered Expression of Bcl-2*

  2004cited by this paper
• BCR-ABL independence and LYN kinase overexpression in chronic myelogenous leukemia cells selected for resistance to STI571.

  2003cited by this paper
• Frequency of major molecular responses to imatinib or interferon alfa plus cytarabine in newly diagnosed chronic myeloid leukemia.

  2003cited by this paper
• Overexpression of P-glycoprotein in K562 cells does not confer resistance to the growth inhibitory effects of imatinib (STI571) in vitro.

  2003cited by this paper
• Prognostic significance of cytogenetic clonal evolution in patients with chronic myelogenous leukemia on imatinib mesylate therapy.

  2003cited by this paper
• Multidrug resistance mediated by the breast cancer resistance protein BCRP (ABCG2)

  2003cited by this paper
• MDR1 gene overexpression confers resistance to imatinib mesylate in leukemia cell line models.

  2003cited by this paper
• Detection of BCR-ABL mutations in patients with CML treated with imatinib is virtually always accompanied by clinical resistance, and mutations in the ATP phosphate-binding loop (P-loop) are associated with a poor prognosis.

  2003cited by this paper
• Several types of mutations of the Abl gene can be found in chronic myeloid leukemia patients resistant to STI571, and they can pre-exist to the onset of treatment.

  2002cited by this paper
• Cytogenetic and Molecular Genetic Evolution of Chronic Myeloid Leukemia

  2002cited by this paper
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  2002cited by this paper
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  2002cited by this paper
• Inviting leukemic cells to waltz with the devil

  2001cited by this paper
• Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification

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  2001cited by this paper
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• Role of 1 Acid Glycoprotein in the In Vivo Resistance of Human BCR-ABL + Leukemic Cells to the Abl Inhibitor STI 571

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