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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

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

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

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

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

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

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

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.

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.

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.

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

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

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.

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

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ASH Publications

American Society of Hematology

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ASH Publications

American Society of Hematology

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