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Journal Articles

Long-Term Efficacy of Dasatinib in Chronic-Phase CML: Results from the Phase I Trial (CA180002).

Jorge Cortes, MD, Charles L. Sawyers, MD, Hagop M. Kantarjian, MD, Neil P. Shah, MD, Ronald Paquette, MD, Prashni Paliwal, Eric Bleickardt, MD, Moshe Talpaz, MD

Blood (2007) 110 (11): 1026.

https://doi.org/10.1182/blood.V110.11.1026.1026

Published: 2007

Journal Articles

PHA-739358, an Aurora Kinase Inhibitor, Induces Clinical Responses in Chronic Myeloid Leukemia Harboring T315I Mutations of BCR-ABL.

Ronald L. Paquette, MD, Neil P. Shah, MD, PhD, Charles L. Sawyers, MD, Giovanni Martinelli, MD, Nicoll John, Meenal Chalukya, Maurizio Rocchetti, PhD, Carina Fiocchi, MD, Sylvia Comis, MD, Laura Capolongo, MD, Bernard Laffranchi, MD

Blood (2007) 110 (11): 1030.

https://doi.org/10.1182/blood.V110.11.1030.1030

Published: 2007

Journal Articles

Sequential Kinase Inhibitor Therapy in CML Patients Can Select for Cells Harboring Compound BCR-ABL Kinase Domain Mutations with Increased Oncogenic Potency: Rationale for Early Combination Therapy of ABL Kinase Inhibitors.

Neil P. Shah, MD, PhD, Brian Skaggs, PhD, Susan Branford, BS, Timothy P. Hughes, MD, John M. Nicoll, BS, Ronald L. Paquette, MD, Charles L. Sawyers, MD

Blood (2006) 108 (11): 751.

https://doi.org/10.1182/blood.V108.11.751.751

Published: 2006

Journal Articles

Potent Transient Inhibition of BCR-ABL by Dasatinib Leads to Complete Cytogenetic Remissions in Patients with Chronic Myeloid Leukemia: Implications for Patient Management and Drug Development.

Neil P. Shah, MD, PhD, John M. Nicoll, BS, Eric Bleickardt, MD, Claude Nicaise, MD, Ronald L. Paquette, MD, Charles L. Sawyers, MD

Blood (2006) 108 (11): 2166.

https://doi.org/10.1182/blood.V108.11.2166.2166

Published: 2006

Journal Articles

The Most Common Dasatinib-Resistant BCR-ABL Kinase Domain Mutations in Patients with Chronic Myeloid Leukemia Are Sensitive to VX-680: Rationale for Early Combination Kinase Inhibitor Therapy.

Neil P. Shah, MD, PhD, Brian Skaggs, PhD, Susan Branford, BS, Timothy P. Hughes, MD, John M. Nicoll, BS, Ronald L. Paquette, MD, Charles L. Sawyers, MD

Blood (2006) 108 (11): 2175.

https://doi.org/10.1182/blood.V108.11.2175.2175

Published: 2006

Journal Articles

Dasatinib (BMS-354825) in Patients with Chronic Myeloid Leukemia (CML) and Philadelphia-Chromosome Positive Acute Lymphoblastic Leukemia (Ph+ ALL) Who Are Resistant or Intolerant to Imatinib: Update of a Phase I Study.

Charles L. Sawyers, H. Kantarjian, N. Shah, J. Cortes, R. Paquette, N. Donato, J. Nicoll, E. Bleickardt, T.-T. Chen, M. Talpaz

Blood (2005) 106 (11): 38.

https://doi.org/10.1182/blood.V106.11.38.38

Published: 2005

Journal Articles

Altered Oncogenic Fitness of Imatinib- and Dasatinib-Resistant BCR-ABL Mutants Is Due to Differential Intrinsic Kinase Activity and Signaling Pathway Selection Defined by Phosphoproteome Profiling.

Brian J. Skaggs, PhD, Michael R. Burgess, PhD, Mercedes E. Gorre, PhD, Thomas G. Graeber, PhD, Charles L. Sawyers, MD

Blood (2005) 106 (11): 692.

https://doi.org/10.1182/blood.V106.11.692.692

Published: 2005

Journal Articles

Good Prognosis of CML Patients with Clonal Cytogenetic Abnormalities in Ph-Negative Cells.

Michael W. Deininger, MD, PhD, Hagop M. Kantarjian, MD, Park Byung, Andreas Hochhaus, MD, Charles L. Sawyers, MD, Michele Baccarani, MD, Insa Gathmann, Charlene So, Brian J. Druker, MD, Francois Guilhot, MD

Blood (2005) 106 (11): 1082.

https://doi.org/10.1182/blood.V106.11.1082.1082

Published: 2005

Journal Articles

Five Year Follow-Up Results of a Phase II Trial in Patients with Late Chronic Phase (L-CP) Chronic Myeloid Leukemia (CML) Treated with Imatinib Who Are Refractory/Intolerant of Interferon-α.

Carlo Gambacorti, Moshe Talpaz, Charles L. Sawyers, Brian J. Druker, Andreas Hochhaus, Charles A. Schiffer, Francois Guilhot, Dietger W. Niederwieser, Richard M. Stone, John M. Goldman, Manisha Mone, Tillmann Krahnke, Insa Gathmann, Hagop M. Kantarjian

Blood (2005) 106 (11): 1089.

https://doi.org/10.1182/blood.V106.11.1089.1089

Published: 2005

Journal Articles

Molecular Analysis of Dasatinib Resistance Mechanisms in CML Patients Identifies Novel BCR-ABL Mutations Predicted To Retain Sensitivity to Imatinib: Rationale for Combination Tyrosine Kinase Inhibitor Therapy.

Neil P. Shah, MD, PhD, John M. Nicoll, Susan Branford, Timothy P. Hughes, MD, Ronald L. Paquette, MD, Moshe Talpaz, MD, Claude Nicaise, MD, Fei Huang, Charles L. Sawyers, MD

Blood (2005) 106 (11): 1093.

https://doi.org/10.1182/blood.V106.11.1093.1093

Published: 2005

Journal Articles

Detection of BCR-ABL kinase mutations in CD34 + cells from chronic myelogenous leukemia patients in complete cytogenetic remission on imatinib mesylate treatment

Su Chu, Helen Xu, Neil P. Shah, David S. Snyder, Stephen J. Forman, Charles L. Sawyers, Ravi Bhatia

Blood (2005) 105 (5): 2093–2098.

https://doi.org/10.1182/blood-2004-03-1114

Published: 2005

Journal Articles

Comparative Analysis of Two BCR-ABL Small Molecule Inhibitors Reveals Overlapping but Distinct Mechanisms of Resistance.

Michael R. Burgess, Neil P. Shah, MD, PhD, Brian J. Skaggs, PhD, Francis Y. Lee, PhD, Charles L. Sawyers, MD

Blood (2004) 104 (11): 552.

https://doi.org/10.1182/blood.V104.11.552.552

Published: 2004

Journal Articles

Imatinib-Resistant BCR-ABL Mutations Alter Oncogenic Potency, Kinase Activity and Substrate Selection.

Mercedes E. Gorre, Ph.D., Brian J. Skaggs, Ph.D., Charles L. Sawyers, M.D.

Blood (2004) 104 (11): 556.

https://doi.org/10.1182/blood.V104.11.556.556

Published: 2004

Journal Articles

Major Cytogenetic Responses to BMS-354825 in Patients with Chronic Myeloid Leukemia Are Associated with a One to Two Log Reduction in BCR-ABL Transcript.

Neil P. Shah, MD, PhD, Susan Branford, Timothy P. Hughes, MD, John M. Nicoll, Arthur P. Decillis, MD, Charles L. Sawyers, MD.

Blood (2004) 104 (11): 1008.

https://doi.org/10.1182/blood.V104.11.1008.1008

Published: 2004

Journal Articles

Hematologic and Cytogenetic Responses in Imatinib-Resistant Chronic Phase Chronic Myeloid Leukemia Patients Treated with the Dual SRC/ABL Kinase Inhibitor BMS-354825: Results from a Phase I Dose Escalation Study.

Charles L. Sawyers, Neil P. Shah, Hagop M. Kantarjian, Nicholas Donato, John Nicoll, Stephen A. Bai, Fei Huang, Edwin Clark, Arthur P. DeCillis, Moshe Talpaz

Blood (2004) 104 (11): 1.

https://doi.org/10.1182/blood.V104.11.1.1

Published: 2004

Journal Articles

BMS-354825 Is a SRC/ABL Inhibitor with High Nanomolar Activity Against the Kit D816v Mutation, Which Drives Systemic Mastocytosis and Is Imatinib-Resistant.

Neil P. Shah, MD, PhD, Francis Y. Lee, PhD, Charles L. Sawyers, MD, Cem Akin, MD, PhD

Blood (2004) 104 (11): 797.

https://doi.org/10.1182/blood.V104.11.797.797

Published: 2004

Journal Articles

Four Years of Follow-Up of 1027 Patients with Late Chronic Phase (L-CP), Accelerated Phase (AP), or Blast Crisis (BC) Chronic Myeloid Leukemia (CML) Treated with Imatinib in Three Large Phase II Trials.

Richard T. Silver, Moshe Talpaz, Charles L. Sawyers, Brian J. Druker, Andreas Hochhaus, Charles A. Schiffer, Francois Guilhot, John M. Goldman, B. Douglas Smith, Manisha Mone, Tillmann Kranhnke, Hagop M. Kantarjian

Blood (2004) 104 (11): 23.

https://doi.org/10.1182/blood.V104.11.23.23

Published: 2004

Journal Articles

Resistance to imatinib: more and more mutations

Charles L. Sawyers

Blood (2003) 102 (1): 4–5.

https://doi.org/10.1182/blood-2003-04-1325

Published: 2003

Journal Articles

Persistence of malignant hematopoietic progenitors in chronic myelogenous leukemia patients in complete cytogenetic remission following imatinib mesylate treatment

Ravi Bhatia, Melissa Holtz, Ning Niu, Rachel Gray, David S. Snyder, Charles L. Sawyers, Daniel A. Arber, Marilyn L. Slovak, Stephen J. Forman

Blood (2003) 101 (12): 4701–4707.

https://doi.org/10.1182/blood-2002-09-2780

Published: 2003

Journal Articles

BCR-ABL point mutants isolated from patients with imatinib mesylate–resistant chronic myeloid leukemia remain sensitive to inhibitors of the BCR-ABL chaperone heat shock protein 90

Mercedes E. Gorre, Katharine Ellwood-Yen, Gabriela Chiosis, Neal Rosen, Charles L. Sawyers

Blood (2002) 100 (8): 3041–3044.

https://doi.org/10.1182/blood-2002-05-1361

Published: 2002

NARROW

Long-Term Efficacy of Dasatinib in Chronic-Phase CML: Results from the Phase I Trial (CA180002).

PHA-739358, an Aurora Kinase Inhibitor, Induces Clinical Responses in Chronic Myeloid Leukemia Harboring T315I Mutations of BCR-ABL.

Sequential Kinase Inhibitor Therapy in CML Patients Can Select for Cells Harboring Compound BCR-ABL Kinase Domain Mutations with Increased Oncogenic Potency: Rationale for Early Combination Therapy of ABL Kinase Inhibitors.

Potent Transient Inhibition of BCR-ABL by Dasatinib Leads to Complete Cytogenetic Remissions in Patients with Chronic Myeloid Leukemia: Implications for Patient Management and Drug Development.

The Most Common Dasatinib-Resistant BCR-ABL Kinase Domain Mutations in Patients with Chronic Myeloid Leukemia Are Sensitive to VX-680: Rationale for Early Combination Kinase Inhibitor Therapy.

Dasatinib (BMS-354825) in Patients with Chronic Myeloid Leukemia (CML) and Philadelphia-Chromosome Positive Acute Lymphoblastic Leukemia (Ph+ ALL) Who Are Resistant or Intolerant to Imatinib: Update of a Phase I Study.

Altered Oncogenic Fitness of Imatinib- and Dasatinib-Resistant BCR-ABL Mutants Is Due to Differential Intrinsic Kinase Activity and Signaling Pathway Selection Defined by Phosphoproteome Profiling.

Good Prognosis of CML Patients with Clonal Cytogenetic Abnormalities in Ph-Negative Cells.

Five Year Follow-Up Results of a Phase II Trial in Patients with Late Chronic Phase (L-CP) Chronic Myeloid Leukemia (CML) Treated with Imatinib Who Are Refractory/Intolerant of Interferon-α.

Molecular Analysis of Dasatinib Resistance Mechanisms in CML Patients Identifies Novel BCR-ABL Mutations Predicted To Retain Sensitivity to Imatinib: Rationale for Combination Tyrosine Kinase Inhibitor Therapy.

Detection of BCR-ABL kinase mutations in CD34 + cells from chronic myelogenous leukemia patients in complete cytogenetic remission on imatinib mesylate treatment

Comparative Analysis of Two BCR-ABL Small Molecule Inhibitors Reveals Overlapping but Distinct Mechanisms of Resistance.

Imatinib-Resistant BCR-ABL Mutations Alter Oncogenic Potency, Kinase Activity and Substrate Selection.

Major Cytogenetic Responses to BMS-354825 in Patients with Chronic Myeloid Leukemia Are Associated with a One to Two Log Reduction in BCR-ABL Transcript.

Hematologic and Cytogenetic Responses in Imatinib-Resistant Chronic Phase Chronic Myeloid Leukemia Patients Treated with the Dual SRC/ABL Kinase Inhibitor BMS-354825: Results from a Phase I Dose Escalation Study.

BMS-354825 Is a SRC/ABL Inhibitor with High Nanomolar Activity Against the Kit D816v Mutation, Which Drives Systemic Mastocytosis and Is Imatinib-Resistant.

Four Years of Follow-Up of 1027 Patients with Late Chronic Phase (L-CP), Accelerated Phase (AP), or Blast Crisis (BC) Chronic Myeloid Leukemia (CML) Treated with Imatinib in Three Large Phase II Trials.

Resistance to imatinib: more and more mutations

Persistence of malignant hematopoietic progenitors in chronic myelogenous leukemia patients in complete cytogenetic remission following imatinib mesylate treatment

BCR-ABL point mutants isolated from patients with imatinib mesylate–resistant chronic myeloid leukemia remain sensitive to inhibitors of the BCR-ABL chaperone heat shock protein 90

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American Society of Hematology

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American Society of Hematology

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