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Targeted CML therapy: controlling drug resistance, seeking cure

Current opinion in genetics & development, 2006-02, Vol.16 (1), p.92-99

2006

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Kinase Domain Mutants of Bcr-Abl Exhibit Altered Transformation Potency, Kinase Activity, and Substrate Utilization, Irrespective of Sensitivity to Imatinib

Molecular and Cellular Biology, 2006-08, Vol.26 (16), p.6082-6093

2006

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Analysis of the Structural Basis of Specificity of Inhibition of the Abl Kinase by STI571

The Journal of biological chemistry, 2002-08, Vol.277 (35), p.32214-32219

2002

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Absence of SKP2 expression attenuates BCR-ABL–induced myeloproliferative disease

Blood, 2008-09, Vol.112 (5), p.1960-1970

2008

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RNAi screening of the tyrosine kinome identifies therapeutic targets in acute myeloid leukemia

Blood, 2008-02, Vol.111 (4), p.2238-2245

2008

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A BCR-ABL mutant lacking direct binding sites for the GRB2, CBL and CRKL adapter proteins fails to induce leukemia in mice

PloS one, 2009-10, Vol.4 (10), p.e7439

2009

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In vitro efficacy of combined treatment depends on the underlying mechanism of resistance in imatinib-resistant Bcr-Abl–positive cell lines

Blood, 2004-01, Vol.103 (1), p.208-215

2004

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Dasatinib (BMS-354825), a dual SRC/ABL kinase inhibitor, inhibits the kinase activity of wild-type, juxtamembrane, and activation loop mutant KIT isoforms associated with human malignancies

Cancer research (Chicago, Ill.), 2006, Vol.66 (1), p.473-481

2006

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Several Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib

Blood, 2003-06, Vol.101 (11), p.4611-4614

2003

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Synergistic Interactions between DMAG and Mitogen-Activated Protein Kinase Kinase 1/2 Inhibitors in Bcr/abl+ Leukemia Cells Sensitive and Resistant to Imatinib Mesylate

Clinical cancer research, 2006-04, Vol.12 (7), p.2239-2247

2006

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Activity of the Bcr-Abl kinase inhibitor PD180970 against clinically relevant Bcr-Abl isoforms that cause resistance to imatinib mesylate (Gleevec, STI571)

Cancer research (Chicago, Ill.), 2002-12, Vol.62 (24), p.7149-7153

2002

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SGX393 inhibits the CML mutant Bcr-AblT315I and preempts in vitro resistance when combined with nilotinib or dasatinib

Proceedings of the National Academy of Sciences - PNAS, 2008-04, Vol.105 (14), p.5507-5512

2008

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KIT Signaling Governs Differential Sensitivity of Mature and Primitive CML Progenitors to Tyrosine Kinase Inhibitors

Cancer research (Chicago, Ill.), 2013-09, Vol.73 (18), p.5775-5786

2013

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Characterization of murine JAK2V617F-positive myeloproliferative disease

Cancer research (Chicago, Ill.), 2006-12, Vol.66 (23), p.11156-11165

2006

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Sensitivity of oncogenic KIT mutants to the kinase inhibitors MLN518 and PD180970

Blood, 2004-12, Vol.104 (12), p.3754-3757

2004

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The BCR-ABL35INS insertion/truncation mutant is kinase-inactive and does not contribute to tyrosine kinase inhibitor resistance in chronic myeloid leukemia

Blood, 2011-11, Vol.118 (19), p.5250-5254

2011

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Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity

The Journal of clinical investigation, 2011-01, Vol.121 (1), p.396-409

2011

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In vitro and in vivo activity of ATP-based kinase inhibitors AP23464 and AP23848 against activation-loop mutants of Kit

Blood, 2005-07, Vol.106 (1), p.227-234

2005

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SGX393 inhibits the CML mutant Bcr-Abl[superscript T315I] and preempts in vitro resistance when combined with nilotinib or dasatinib

Proceedings of the National Academy of Sciences - PNAS, 2008-04, Vol.105 ((14) ; 04, 2008)

2008

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Suppression of CML Progenitor but Not Stem Cells Requires Simultaneous Inhibition of KIT and BCR-ABL1

Blood, 2012-11, Vol.120 (21), p.2778-2778

2012

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Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity

The Journal of clinical investigation, 2011-03, Vol.121 (3), p.1222-1222

2011

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Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity.(Research article)

The Journal of clinical investigation, 2011-01, Vol.121 (1), p.396

2011

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Suppression of CML Progenitor but Not CML Stem Cell Growth Requires Dual Inhibition of BCR-ABL and KIT

Blood, 2008-11, Vol.112 (11), p.190-190

2008

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SGX393 inhibits the CML mutant Bcr-Abl T315I and preempts in vitro resistance when combined with nilotinib or dasatinib

Proceedings of the National Academy of Sciences - PNAS, 2008-04, Vol.105 (14), p.5507-5512

2008

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Targeted CML therapy: controlling drug resistance, seeking cure

Kinase Domain Mutants of Bcr-Abl Exhibit Altered Transformation Potency, Kinase Activity, and Substrate Utilization, Irrespective of Sensitivity to Imatinib

Analysis of the Structural Basis of Specificity of Inhibition of the Abl Kinase by STI571

Absence of SKP2 expression attenuates BCR-ABL–induced myeloproliferative disease

RNAi screening of the tyrosine kinome identifies therapeutic targets in acute myeloid leukemia

A BCR-ABL mutant lacking direct binding sites for the GRB2, CBL and CRKL adapter proteins fails to induce leukemia in mice

AP24534, a Pan-BCR-ABL Inhibitor for Chronic Myeloid Leukemia, Potently Inhibits the T315I Mutant and Overcomes Mutation-Based Resistance

In vitro efficacy of combined treatment depends on the underlying mechanism of resistance in imatinib-resistant Bcr-Abl–positive cell lines

Dasatinib (BMS-354825), a dual SRC/ABL kinase inhibitor, inhibits the kinase activity of wild-type, juxtamembrane, and activation loop mutant KIT isoforms associated with human malignancies

Several Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib

Synergistic Interactions between DMAG and Mitogen-Activated Protein Kinase Kinase 1/2 Inhibitors in Bcr/abl+ Leukemia Cells Sensitive and Resistant to Imatinib Mesylate

Activity of the Bcr-Abl kinase inhibitor PD180970 against clinically relevant Bcr-Abl isoforms that cause resistance to imatinib mesylate (Gleevec, STI571)

SGX393 inhibits the CML mutant Bcr-AblT315I and preempts in vitro resistance when combined with nilotinib or dasatinib

KIT Signaling Governs Differential Sensitivity of Mature and Primitive CML Progenitors to Tyrosine Kinase Inhibitors

Characterization of murine JAK2V617F-positive myeloproliferative disease

Sensitivity of oncogenic KIT mutants to the kinase inhibitors MLN518 and PD180970

The BCR-ABL35INS insertion/truncation mutant is kinase-inactive and does not contribute to tyrosine kinase inhibitor resistance in chronic myeloid leukemia

Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity

In vitro and in vivo activity of ATP-based kinase inhibitors AP23464 and AP23848 against activation-loop mutants of Kit

SGX393 inhibits the CML mutant Bcr-Abl[superscript T315I] and preempts in vitro resistance when combined with nilotinib or dasatinib

Suppression of CML Progenitor but Not Stem Cells Requires Simultaneous Inhibition of KIT and BCR-ABL1

Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity

Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity.(Research article)

Suppression of CML Progenitor but Not CML Stem Cell Growth Requires Dual Inhibition of BCR-ABL and KIT

SGX393 inhibits the CML mutant Bcr-Abl T315I and preempts in vitro resistance when combined with nilotinib or dasatinib

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