Molecular Mechanisms of Resistance to Tyrosine Kinase Inhibitors

No abstract is available for this paper.

• Publication year

  2019

• Venue

  Current Hematologic Malignancy Reports

• Publication date

  2019-08-28

• Fields of study

  Medicine

• Identifiers
  DOI 10.1007/s11899-019-00543-7PMID 31463864
• 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.

• Chronic Myeloid Leukemia, Version 1.2019, NCCN Clinical Practice Guidelines in Oncology.

  2018cited by this paper
• Chronic myeloid leukemia: the paradigm of targeting oncogenic tyrosine kinase signaling and counteracting resistance for successful cancer therapy

  2018cited by this paper
• Mechanisms of Resistance to ABL Kinase Inhibition in Chronic Myeloid Leukemia and the Development of Next Generation ABL Kinase Inhibitors.

  2017cited by this paper
• Resistance in chronic myeloid leukemia: definitions and novel therapeutic agents

  2017cited by this paper
• Molecular monitoring of chronic myeloid leukemia: present and future

  2016cited by this paper
• European LeukemiaNet recommendations for the management and avoidance of adverse events of treatment in chronic myeloid leukaemia

  2016cited by this paper
• Next-generation sequencing for sensitive detection of BCR-ABL1 mutations relevant to tyrosine kinase inhibitor choice in imatinib-resistant patients

  2016cited by this paper
• Tyrosine Kinase Inhibitors in Ph+ Chronic Myeloid Leukemia Therapy: a Review.

  2016cited by this paper
• New Methodologies in the Molecular Monitoring of CML

  2016cited by this paper
• Mechanisms of resistance to BCR-ABL TKIs and the therapeutic strategies: A review.

  2015cited by this paper
• BCR-ABL1 mutation development during first-line treatment with dasatinib or imatinib for chronic myeloid leukemia in chronic phase

  2015cited by this paper
• Causes of resistance and treatment choices of second- and third-line treatment in chronic myelogenous leukemia patients

  2015cited by this paper
• Ponatinib is not transported by ABCB1, ABCG2 or OCT-1 in CML cells

  2015cited by this paper
• Next-generation deep sequencing improves detection of BCR-ABL1 kinase domain mutations emerging under tyrosine kinase inhibitor treatment of chronic myeloid leukemia patients in chronic phase

  2015cited by this paper
• Chronic Myeloid Leukemia: Advances in Understanding Disease Biology and Mechanisms of Resistance to Tyrosine Kinase Inhibitors

  2015cited by this paper
• Interaction of the Efflux Transporters ABCB1 and ABCG2 With Imatinib, Nilotinib, and Dasatinib

  2014cited by this paper
• Combined STAT3 and BCR-ABL1 Inhibition Induces Synthetic Lethality in Therapy-Resistant Chronic Myeloid Leukemia

  2014cited by this paper
• Structure, function, and resistance in chronic myeloid leukemia.

  2014cited by this paper
• A therapeutically targetable mechanism of BCR-ABL–independent imatinib resistance in chronic myeloid leukemia

  2014cited by this paper
• The clinical significance of ABCC3 as an imatinib transporter in chronic myeloid leukaemia

  2014cited by this paper
• Implications of BCR-ABL1 kinase domain-mediated resistance in chronic myeloid leukemia.

  2014cited by this paper
• Adherence and Persistence Among Chronic Myeloid Leukemia Patients During Second-Line Tyrosine Kinase Inhibitor Treatment

  2014cited by this paper
• BCR-ABL1 compound mutations combining key kinase domain positions confer clinical resistance to ponatinib in Ph chromosome-positive leukemia.

  2014cited by this paper
• Early response with dasatinib or imatinib in chronic myeloid leukemia: 3-year follow-up from a randomized phase 3 trial (DASISION).

  2014cited by this paper
• Role of anti-apoptotic pathways activated by BCR/ABL in the resistance of chronic myeloid leukemia cells to tyrosine kinase inhibitors.

  2013cited by this paper
• Unraveling the complexity of tyrosine kinase inhibitor-resistant populations by ultra-deep sequencing of the BCR-ABL kinase domain.

  2013cited by this paper
• Mechanisms of resistance to BCR-ABL and other kinase inhibitors.

  2013cited by this paper
• Early molecular response and female sex strongly predict stable undetectable BCR-ABL1, the criteria for imatinib discontinuation in patients with CML.

  2013cited by this paper
• BCR-ABL1 compound mutations in tyrosine kinase inhibitor-resistant CML: frequency and clonal relationships.

  2013cited by this paper
• Activity of ponatinib against clinically-relevant AC220-resistant kinase domain mutants of FLT3-ITD.

  2013cited by this paper
• European LeukemiaNet recommendations for the management of chronic myeloid leukemia: 2013.

  2013cited by this paper
• Chronic myeloid leukemia stem cells are not dependent on Bcr-Abl kinase activity for their survival.

  2012cited by this paper
• Chronic myeloid leukemia: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up.

  2012cited by this paper
• Dasatinib or imatinib in newly diagnosed chronic-phase chronic myeloid leukemia: 2-year follow-up from a randomized phase 3 trial (DASISION).

  2012cited by this paper
• Ponatinib in refractory Philadelphia chromosome-positive leukemias.

  2012cited by this paper
• Nilotinib vs imatinib in patients with newly diagnosed Philadelphia chromosome-positive chronic myeloid leukemia in chronic phase: ENESTnd 3-year follow-up

  2012cited by this paper
• A randomized trial of dasatinib 100 mg versus imatinib 400 mg in newly diagnosed chronic-phase chronic myeloid leukemia.

  2012cited by this paper
• Chronic lymphocytic leukemia: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up.

  2011cited by this paper
• BCR-ABL kinase domain mutation analysis in chronic myeloid leukemia patients treated with tyrosine kinase inhibitors: recommendations from an expert panel on behalf of European LeukemiaNet.

  2011cited by this paper
• Health-related quality of life in chronic myeloid leukemia patients receiving long-term therapy with imatinib compared with the general population.

  2011cited by this paper
• Comprehensive analysis of kinase inhibitor selectivity

  2011cited by this paper
• Nilotinib versus imatinib for the treatment of patients with newly diagnosed chronic phase, Philadelphia chromosome-positive, chronic myeloid leukaemia: 24-month minimum follow-up of the phase 3 randomised ENESTnd trial.

  2011cited by this paper
• Functional activity of the OCT-1 protein is predictive of long-term outcome in patients with chronic-phase chronic myeloid leukemia treated with imatinib.

  2010cited by this paper
• Poor adherence is the main reason for loss of CCyR and imatinib failure for chronic myeloid leukemia patients on long-term therapy.

  2010cited by this paper
• Impact of additional chromosomal aberrations and BCR-ABL kinase domain mutations on the response to nilotinib in Philadelphia chromosome-positive chronic myeloid leukemia

  2010cited by this paper
• BCR-ABL tyrosine kinase inhibitors in the treatment of Philadelphia chromosome positive chronic myeloid leukemia: a review.

  2010cited by this paper
• Chronic myeloid leukemia: mechanisms of blastic transformation.

  2010cited by this paper
• Dasatinib in imatinib‐resistant or imatinib‐intolerant chronic myeloid leukemia in blast phase after 2 years of follow‐up in a phase 3 study

  2010cited by this paper
• Dasatinib versus imatinib in newly diagnosed chronic-phase chronic myeloid leukemia.

  2010cited by this paper
• Chronic myeloid leukemia: an update of concepts and management recommendations of European LeukemiaNet.

  2009cited by this paper
• AP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistance.

  2009cited by this paper
• Mechanisms of Resistance to Imatinib and Second-Generation Tyrosine Inhibitors in Chronic Myeloid Leukemia

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

  2009cited by this paper
• Targeting cancer with small molecule kinase inhibitors

  2009cited by this paper
• Solution Conformations and Dynamics of ABL Kinase-Inhibitor Complexes Determined by NMR Substantiate the Different Binding Modes of Imatinib/Nilotinib and Dasatinib*♦

  2008cited by this paper
• Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia.

  2007cited by this paper
• 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
• Important Therapeutic Targets in Chronic Myelogenous Leukemia

  2007cited by this paper
• Effect of Cellular Quiescence on the Success of Targeted CML Therapy

  2007cited by this paper
• Trough imatinib plasma levels are associated with both cytogenetic and molecular responses to standard-dose imatinib in chronic myeloid leukemia.

  2007cited by this paper
• Chronic myeloid leukaemia as a model of disease evolution in human cancer

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

  2007cited by this paper
• Molecular monitoring of BCR-ABL as a guide to clinical management in chronic myeloid leukaemia.

  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
• Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia.

  2006cited by this paper
• Frequency and clinical significance of BCR-ABL mutations in patients with chronic myeloid leukemia treated with imatinib mesylate

  2006cited by this paper
• AMN107 (nilotinib): a novel and selective inhibitor of BCR-ABL

  2006cited by this paper
• Phosphorylation of the ATP-binding loop directs oncogenicity of drug-resistant BCR-ABL mutants

  2006cited by this paper
• Clinical Pharmacokinetics of Imatinib

  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
• Response and resistance in 300 patients with BCR‐ABL–positive leukemias treated with imatinib in a single center

  2005cited by this paper
• Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl.

  2005cited by this paper
• Real-time quantitative PCR analysis can be used as a primary screen to identify patients with CML treated with imatinib who have BCR-ABL kinase domain mutations.

  2004cited by this paper
• Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia.

  2003cited by this paper
• Mechanisms of resistance to STI571 in Philadelphia chromosome-associated leukemias

  2003cited by this paper
• Resistance of Philadelphia-chromosome positive leukemia towards the kinase inhibitor imatinib (STI571, Glivec): a targeted oncoprotein strikes back

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

  2003cited by this paper
• Imatinib mesylate (STI571) therapy for Philadelphia chromosome-positive chronic myelogenous leukemia in blast phase.

  2002cited by this paper
• Imatinib induces hematologic and cytogenetic responses in patients with chronic myelogenous leukemia in myeloid blast crisis: results of a phase II study.

  2002cited by this paper
• Oncogenic tyrosine kinases and the dna-damage response

  2002cited by this paper
• Molecular and chromosomal mechanisms of resistance to imatinib (STI571) therapy

  2002cited by this paper
• Mechanisms of cancer drug resistance.

  2002cited by this paper
• 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.

  2002cited by this paper
• Phosphorylation and structure-based functional studies reveal a positive and a negative role for the activation loop of the c-Abl tyrosine kinase

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

  2001cited by this paper
• c-Abl Has High Intrinsic Tyrosine Kinase Activity That Is Stimulated by Mutation of the Src Homology 3 Domain and by Autophosphorylation at Two Distinct Regulatory Tyrosines*

  2000cited by this paper
• Cytochrome P4503A (CYP3A) metabolism: Prediction ofIn Vivo activity in humans

  1996cited by this paper
• A cellular oncogene is translocated to the Philadelphia chromosome in chronic myelocytic leukaemia

  1982cited by this paper
• Pu.1-dependent Transcription Gata-1 Interacts with the Myeloid Pu.1 Transcription Factor and Represses

  year unknowncited by this paper

• Analyzing Two Decades of Leukemia Mortality in the U.S. (1999-2020).

  2025cites this paper
• Targeted inactivation of EWSR1 : : FLI1 gene in Ewing sarcoma via CRISPR/Cas9 driven by an Ewing-specific GGAA promoter

  2025cites this paper
• Chronic Myeloid Leukemia and the T315I BCR::ABL1 Mutation

  2025cites this paper
• Unique Gender-Related Characteristics and Differences of Chronic Myeloid Leukemia Patients in Azerbaijan: A Retrospective Cohort Study

  2025cites this paper
• Biomarker Testing for Guiding Precision Medicine for Patients with Non-Small Cell Lung Cancer.

  2024cites this paper
• Getting the right combination to break the epigenetic code

  2024cites this paper
• Mechanisms underlying therapeutic resistance of tyrosine kinase inhibitors in chronic myeloid leukemia

  2024influential citation
• Combination of an aurora kinase inhibitor and the ABL tyrosine kinase inhibitor asciminib against ABL inhibitor-resistant CML cells

  2024cites this paper
• The importance of personalized medicine in chronic myeloid leukemia management: a narrative review

  2023cites this paper
• Oncogene-addicted metastatic non-small-cell lung cancer: ESMO Clinical Practice Guideline for diagnosis, treatment and follow-up.

  2023cites this paper
• 5-Oxohexahydroquinolines bearing 4-pyridyl methyl carboxylate as P-glycoprotein inhibitors and multidrug resistance reversal agents in cancer cells

  2023cites this paper
• Effects of Imatinib and Artemisia vulgaris extracts in combination on leukemia cell proliferation

  2023cites this paper
• Derivates of 1,6-dihyadroazaazulenes as inhibitors of tyrosine kinases BCR-ABL1 wild type and mutant T315I: a molecular dynamics approach

  2023cites this paper
• Anticancer perspective of 6-shogaol: anticancer properties, mechanism of action, synergism and delivery system

  2023cites this paper
• Association of CYP3A5*3, CYP3A4*18 & CYP2B6*6 polymorphisms with imatinib treatment outcome in Azerbaijani chronic myeloid leukaemia patients

  2023cites this paper
• Advances in Nanopore and Photoelectron-Based High-Throughput Sequencing Technology for Single-Molecule Sequencing

  2023cites this paper
• Precision Deuteration in Search of Anticancer Agents: Approaches to Cancer Drug Discovery

  2023cites this paper
• HDAC inhibitor chidamide overcomes drug resistance in chronic myeloid leukemia with the T315i mutation through the Akt–autophagy pathway

  2023cites this paper
• Resistance Mechanisms in Pediatric B-Cell Acute Lymphoblastic Leukemia

  2022cites this paper
• Recent Advances in Treatment Options for Childhood Acute Lymphoblastic Leukemia

  2022cites this paper
• Mechanisms of Resistance and Implications for Treatment Strategies in Chronic Myeloid Leukaemia

  2022cites this paper
• Protein Tyrosine Kinases: Their Roles and Their Targeting in Leukemia

  2021cites this paper
• Mathematical and Systems Medicine Approaches to Resistance Evolution and Prevention in Cancer

  2021cites this paper
• Resistance to Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia—From Molecular Mechanisms to Clinical Relevance

  2021cites this paper
• Precision diagnostics: Integration of tissue pathology and genomics in cancer.

  2021cites this paper
• Kinase Inhibition in Relapsed/Refractory Leukemia and Lymphoma Settings: Recent Prospects into Clinical Investigations

  2021cites this paper
• Icaritin induces cellular senescence by accumulating the ROS production and regulation of the Jak2/Stat3/p21 pathway in imatinib-resistant, chronic myeloid leukemia cells.

  2021cites this paper
• Detection of mutations in CML patients resistant to tyrosine kinase inhibitor: imatinib mesylate therapy

  2021cites this paper
• Therapeutic Potential of EWSR1–FLI1 Inactivation by CRISPR/Cas9 in Ewing Sarcoma

  2021cites this paper
• The effect of Gö6976 on chronic myeloid leukemia in vitro and in vivo

  2021cites this paper
• Synthesis, molecular modeling, and biological evaluation of novel imatinib derivatives as anticancer agents

  2021cites this paper
• A graphical, interactive and GPU-enabled workflow to process long-read sequencing data

  2021cites this paper
• The Use of Inhibitors of Tyrosine Kinase in Paediatric Haemato-Oncology—When and Why?

  2021cites this paper
• Combination Therapies in Chronic Myeloid Leukemia for Potential Treatment-Free Remission: Focus on Leukemia Stem Cells and Immune Modulation

  2021cites this paper
• Discovery of new pyrimidopyrrolizine/indolizine-based derivatives as P-glycoprotein inhibitors: Design, synthesis, cytotoxicity, and MDR reversal activities.

  2021cites this paper
• miRNAs Mediated Drug Resistance in Hematological Malignancies.

  2021cites this paper
• Cytotoxic effect of 6-Shogaol in Imatinib sensitive and resistant K562 cells

  2021cites this paper
• Hypoxia Induces Resistance to EGFR Inhibitors in Lung Cancer Cells via Upregulation of FGFR1 and the MAPK Pathway

  2020cites this paper
• Improvement of conventional anti-cancer drugs as new tools against multidrug resistant tumors.

  2020cites this paper
• Novel strategies to eradicate resistant cells in chronic myeloid leukemia.

  2020cites this paper
• Therapeutic Challenges in Chronic Myeloid Leukemia: A Case-Based Discussion

  2020cites this paper
• In Vitro Comparison of the Effects of Imatinib and Ponatinib on Chronic Myeloid Leukemia Progenitor/Stem Cell Features

  2020cites this paper
• Extracellular vesicles as a novel source of biomarkers in liquid biopsies for monitoring cancer progression and drug resistance.

  2019cites this paper