Associated Papers
BCR-ABL kinase domain mutations in CML patients, experience from a tertiary care center in North India.
S A et al.
Leukemia Research Reports, 2024
Spectrum of BCR-ABL Mutations and Treatment Outcomes in Ethiopian Imatinib-Resistant Patients With Chronic Myeloid Leukemia.
Tadesse F et al.
Jco Global Oncology, 2021
Novel mutations in the kinase domain of BCR-ABL gene causing imatinib resistance in chronic myeloid leukemia patients.
Chandrasekhar C et al.
Scientific Reports, 2019
Single-Molecule Sequencing Reveals Patterns of Preexisting Drug Resistance That Suggest Treatment Strategies in Philadelphia-Positive Leukemias.
Schmitt MW et al.
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research, 2018
Comparison of Frequency and Sensitivity of BCR-ABL1 Kinase Domain Mutations in Asian and White Patients With Imatinib-resistant Chronic-Phase Chronic Myeloid Leukemia.
Kim H et al.
Clinical Lymphoma, Myeloma & Leukemia, 2018
Characteristics of BCR-ABL kinase domain mutations in chronic myeloid leukemia from India: not just missense mutations but insertions and deletions are also associated with TKI resistance.
Patkar N et al.
Leukemia & Lymphoma, 2016
Compound mutations in BCR-ABL1 are not major drivers of primary or secondary resistance to ponatinib in CP-CML patients.
Deininger MW et al.
Blood, 2016
Treatment of chronic myelogenous leukemia.
Kujak C et al.
American Journal of Health-system Pharmacy : Ajhp : Official Journal of the American Society of Health-system Pharmacists, 2016
[Dasatinib treatment based on BCR- ABL mutation detection in imatinib- resistant patients with chronic myeloid leukemia].
Jiang Q et al.
Zhonghua Xue Ye Xue Za Zhi = Zhonghua Xueyexue Zazhi, 2016
Sensitive detection of pre-existing BCR-ABL kinase domain mutations in CD34+ cells of newly diagnosed chronic-phase chronic myeloid leukemia patients is associated with imatinib resistance: implications in the post-imatinib era.
Iqbal Z et al.
Plos One, 2013
Role of treatment in the appearance and selection of BCR-ABL1 kinase domain mutations.
Razga F et al.
Molecular Diagnosis & Therapy, 2012
Bcr-Abl dependent post-transcriptional activation of NME2 expression is a specific and common feature of chronic myeloid leukemia.
Tschiedel S et al.
Leukemia & Lymphoma, 2012
Conformational control inhibition of the BCR-ABL1 tyrosine kinase, including the gatekeeper T315I mutant, by the switch-control inhibitor DCC-2036.
Chan WW et al.
Cancer Cell, 2011
Impact of BCR-ABL mutations on patients with chronic myeloid leukemia.
Hochhaus A et al.
Cell Cycle (georgetown, Tex.), 2011
The durable clearance of the T315I BCR-ABL mutated clone in chronic phase chronic myelogenous leukemia patients on omacetaxine allows tyrosine kinase inhibitor rechallenge.
Nicolini FE et al.
Clinical Lymphoma, Myeloma & Leukemia, 2010
Mutations in ABL kinase domain are associated with inferior progression-free survival.
Sharma P et al.
Leukemia & Lymphoma, 2010
Choosing the best treatment strategy for chronic myeloid leukemia patients resistant to imatinib: weighing the efficacy and safety of individual drugs with BCR-ABL mutations and patient history.
Jabbour E et al.
Leukemia, 2010
Dasatinib treatment of chronic-phase chronic myeloid leukemia: analysis of responses according to preexisting BCR-ABL mutations.
Müller MC et al.
Blood, 2009
Long-term outcome of patients with chronic myeloid leukemia treated with second-generation tyrosine kinase inhibitors after imatinib failure is predicted by the in vitro sensitivity of BCR-ABL kinase domain mutations.
Jabbour E et al.
Blood, 2009
A co-operative evaluation of different methods of detecting BCR-ABL kinase domain mutations in patients with chronic myeloid leukemia on second-line dasatinib or nilotinib therapy after failure of imatinib.
Ernst T et al.
Haematologica, 2009
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.
Branford S et al.
Blood, 2003