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BLOOD (2009)
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
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BLOOD (2008)
The biologic properties of leukemias arising from BCR/ABL-mediated transformation vary as a function of developmental origin and activity of the p19ARF gene
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BLOOD (2008)
Failure of CDKN2A/B (INK4A/B-ARF)-mediated tumor suppression and resistance to targeted therapy in acute lymphoblastic leukemia induced by BCR-ABL
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Dasatinib treatment can overcome imatinib and nilotinib resistance in CML patient carrying F359I mutation of BCR-ABL oncogene
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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
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Intermittent target inhibition with dasatinib 100 mg once daily preserves efficacy and improves tolerability in imatinib-resistant and -intolerant chronic-phase chronic myeloid leukemia
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Association between imatinib-resistant BCR-ABL mutation-negative leukemia and persistent activation of LYN kinase
Ji Wu et al.
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Quantitative monitoring of cell clones carrying point mutations in the BCR-ABL tyrosine kinase domain by ligation-dependent polymerase chain reaction (LD-PCR)
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Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is active in patients with imatinib-resistant or -intolerant accelerated-phase chronic myelogenous leukemia
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Quantitative monitoring by polymerase colony assay of known mutations resistant to ABL kinase inhibitors
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BLOOD (2007)
Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is effective in patients with Philadelphia chromosome-positive chronic myelogenous leukemia in chronic phase following imatinib resistance and intolerance
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BLOOD (2007)
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Sequential ABL kinase inhibitor therapy selects for compound drug-resistant BCR-ABL mutations with altered oncogenic potency
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Kinase domain mutations of BCR-ABL frequently precede imatinib-based therapy and give rise to relapse in patients with de novo Philadelphia-positive acute lymphoblastic leukemia (Ph+ ALL)
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BLOOD (2007)
Identification of BCR-ABL point mutations conferring resistance to the Abl kinase inhibitor AMN107 (nilotinib) by a random mutagenesis study
Arghya Ray et al.
BLOOD (2007)
Dasatinib induces significant hematologic and cytogenetic responses in patients with imatinib-resistant or -intolerant chronic myeloid leukemia in accelerated phase
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Dasatinib induces complete hematologic and cytogenetic responses in patients with imatinib-resistant or -intolerant chronic myeloid leukemia in blast crisis
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BLOOD (2007)
Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy
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BLOOD (2007)
Resistance to dasatinib in Philadelphia-positive leukemia patients and the presence or the selection of mutations at residues 315 and 317 in the BCR-ABL kinase domain
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Mutations of the BCR-ABL-kinase domain occur in a minority of patients with stable complete cytogenetic response to imatinib
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High-throughput, sensitive and quantitative assay for the detection of BCR-ABL kinase domain mutations
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Phosphorylation of the ATP-binding loop directs oncogenicity of drug-resistant BCR-ABL mutants
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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
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Targeting multiple kinase pathways in leukemic progenitors and stem cells is essential for improved treatment of Ph+ leukemia in mice
Yiguo Hu et al.
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Comparison of imatinib, mesylate, dasatinib (BMS-354825), and nilotinib (AMN107) in an N-ethyl-N-nitrosourea (ENU)-based mutagenesis screen:: high efficacy of drug combinations
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BLOOD (2006)
Frequency and clinical significance of BCR-ABL mutations in patients with chronic myeloid leukemia treated with imatinib mesylate
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Evolving concepts in the management of chronic myeloid leukemia: recommendations from an expert panel on behalf of the European LeukemiaNet
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BLOOD (2006)
Bcr-Abl resistance screening predicts a limited spectrum of point mutations to be associated with clinical resistance to the AN kinase inhibitor nilotinib (AMN107)
Nikolas von Bubnoff et al.
BLOOD (2006)
Kinase domain mutants of Bcr-Abl exhibit altered transformation potency, kinase activity, and substrate utilization, irrespective of sensitivity to imatinib
Ian J. Griswold et al.
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AMN107 (nilotinib): a novel and selective inhibitor of BCR-ABL
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BRITISH JOURNAL OF CANCER (2006)
Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias
Moshe Talpaz et al.
NEW ENGLAND JOURNAL OF MEDICINE (2006)
Nilotinib in imatinib-resistant CML and Philadelphia chromosome-positive ALL
Hagop Kantarjian et al.
NEW ENGLAND JOURNAL OF MEDICINE (2006)
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The Bcr-Abl mutations T315I and Y253H do not confer a growth advantage in the absence of imatinib
C Miething et al.
LEUKEMIA (2006)
The presence of a BCR-ABL mutant allele in CML does not always explain clinical resistance to imatinib
JS Khorashad et al.
LEUKEMIA (2006)
Advances in the structural biology, design and clinical development of Bcr-Abl kinase inhibitors for the treatment of chronic myeloid leukaemia
PW Manley et al.
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Selecting and deselecting imatinib-resistant clones:: observations made by longitudinal, quantitative monitoring of mutated BCR-ABL
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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
SG Willis et al.
BLOOD (2005)
ABL mutations in late chronic phase chronic myeloid leukemia patients with up-front cytogenetic resistance to imatinib are associated with a greater likelihood of progression to blast crisis and shorter survival: A study by the GIMEMA working party on chronic myeloid leukemia
S Soverini et al.
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In vitro activity of Bcr-Abl inhibitors AMN107 and BMS-354825 against clinically relevant imatinib-resistant Abl kinase domain mutants
T O'Hare et al.
CANCER RESEARCH (2005)
Comparative analysis of two clinically active BCR-ABL kinase inhibitors reveals the role of conformation-specific binding in resistance
MR Burgess et al.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2005)
Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl
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Requirement of Src kinases Lyn, Hck and Fgr for BCR-ABL1-induced B-lymphoblastic leukemia but not chronic myeloid leukemia
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MINI-REVIEWS IN MEDICINAL CHEMISTRY (2004)
Discovery of N-(2-chloro-6-methylphenyl)-2-(6-(4-(2-hydroxyethyl)-piperazin-1-yl)-2-methylpyrimidin-4-ylamino)thiazole-5-carboxamide (BMS-354825), a dual Src/Abl kinase inhibitor with potent antitumor activity in preclinical assays
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V Nardi et al.
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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
S Branford et al.
BLOOD (2003)
Several Bcr-Ab1 kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib
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BLOOD (2003)
Mechanisms of autoinhibition and STI-571/imatinib resistance revealed by mutagenesis of BCR-ABL
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CELL (2003)
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Sensitive and quantitative detection of mutations associated with clinical resistance to STI-571
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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
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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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BLOOD (2002)
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Ph+ acute lymphoblastic leukemia resistant to the tyrosine kinase inhibitor STI571 has a unique BCR-ABL gene mutation
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BLOOD (2002)
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