High frequency of point mutations clustered within the adenosine triphosphate-binding region of BCR/ABL in patients with chronic myeloid leukemia or Ph-positive acute lymphoblastic leukemia who develop imatinib (STI571) resistance.
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Summary
A high frequency of mutations clustered within the ATP-binding region of BCR/ABL in resistant patients is confirmed and may allow intervention before relapse by identifying emerging mutations with defined impacts on imatinib binding.
- Type
- article
- Published
- 2002-05-01
- Cited by
- 708
- References
- 17
- Access
- Open access
- OpenAlex
- https://openalex.org/W1968071128
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:28016381
Keywords
Imatinib, Myeloid leukemia, Point mutation, Imatinib mesylate, Cancer research
References
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- 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*
- Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification
- Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr–Abl positive cells
- Mechanisms of resistance imatinib (STI571) in preclinical models and in leukemia patients.
- Monitoring chronic myeloid leukaemia therapy by real‐time quantitative PCR in blood is a reliable alternative to bone marrow cytogenetics
- An Activating Mutation in the ATP Binding Site of the ABL Kinase Domain*
- Structural mechanism for STI-571 inhibition of abelson tyrosine kinase.
- A novel BCR–ABL transcript (e8a2) with the insertion of an inverted sequence of ABL intron 1b in a patient with Philadelphia‐positive chronic myeloid leukaemia
- Mechanism of resistance to the ABL tyrosine kinase inhibitor STI571 in BCR/ABL-transformed hematopoietic cell lines.
- Activity of a specific inhibitor of the BCR-ABL tyrosine kinase in the blast crisis of chronic myeloid leukemia and acute lymphoblastic leukemia with the Philadelphia chromosome.
- Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia.
- Roots of Clinical Resistance to STI-571 Cancer Therapy
Cited by
- Finding the next Gleevec: FLT3 targeted kinase inhibitor therapy for acute myeloid leukemia.
- Molecular mechanisms of resistance of leukemia to imatinib mesylate.
- Denaturing-HPLC-based assay for detection of ABL mutations in chronic myeloid leukemia patients resistant to Imatinib.
- Detection and Monitoring of SARS Coronavirus in the Plasma and Peripheral Blood Lymphocytes of Patients with Severe Acute Respiratory Syndrome
- FLT3-ITD-TKD dual mutants associated with AML confer resistance to FLT3 PTK inhibitors and cytotoxic agents by overexpression of Bcl-x(L).
- Limited clinical value of regular bone marrow cytogenetic analysis in imatinib-treated chronic phase CML patients monitored by RQ-PCR for BCR-ABL
- Part I: mechanisms of resistance to imatinib in chronic myeloid leukaemia.
- Dasatinib induces complete cytogenetic response and loss of F359C in an imatinib resistant chronic myelocytic leukemia patient
- Detection of BCR-ABL mutations and resistance to imatinib mesylate.
- Front-line TKI therapy for chronic-phase CML: the luxury of choice.
- Standard treatment of Ph+ CML in 2010: how, when and where not to use what BCR/ABL1 kinase inhibitor?
- Clinical outcome of chronic myeloid leukemia imatinib-resistant patients: do BCR–ABL kinase domain mutations affect patient survival? First multicenter Argentinean study
- Genetic determinants of anticancer drug activity: towards a global approach to personalized cancer medicine
- Unintentional Weakness of Cancers: The MEK–ERK Pathway as a Double-Edged Sword
- What a Tangled Web We Weave: Emerging Resistance Mechanisms to Inhibition of the Phosphoinositide 3-kinase Pathway
- Relationship between SLCO1B3 and ABCA3 polymorphisms and imatinib response in chronic myeloid leukemia patients
- THE ROLE OF SRC FAMILY TYROSINE KINASES IN BCR-ABL SIGNAL TRANSDUCTION AND CHRONIC MYELOGENOUS LEUKEMIA
- Molecularly targeted treatment of chronic myeloid leukemia: beyond the imatinib era.
- Molecular Matchmaking: A Computational Study of the Electrostatic Interaction Between Chronic Myeloid Leukemia Drugs and Bcr-Abl Oncoprotein
- BCRABL Transcript Detection by Quantitative Real-Time PCR
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