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Journal Articles

STAT5 signaling is required for the efficient induction and maintenance of CML in mice

Dan Ye, Nicholas Wolff, Li Li, Shumin Zhang, Robert L. Ilaria, Jr

Blood (2006) 107 (12): 4917–4925.

https://doi.org/10.1182/blood-2005-10-4110

Published: 2006

Journal Articles

PD166326, a novel tyrosine kinase inhibitor, has greater antileukemic activity than imatinib mesylate in a murine model of chronic myeloid leukemia

Nicholas C. Wolff, Darren R. Veach, William P. Tong, William G. Bornmann, Bayard Clarkson, Robert L. Ilaria, Jr

Blood (2005) 105 (10): 3995–4003.

https://doi.org/10.1182/blood-2004-09-3534

Published: 2005

Journal Articles

STAT5 and STAT5A Signaling Play an Important Role in the Pathophysiology of the CML-Like Myeloproliferative Disorder in Mice.

Dan Ye, MD, Li Li, MD, Robert L. Ilaria, Jr., MD

Blood (2004) 104 (11): 2959.

https://doi.org/10.1182/blood.V104.11.2959.2959

Published: 2004

Journal Articles

The CNS is a sanctuary for leukemic cells in mice receiving imatinib mesylate for Bcr/Abl-induced leukemia

Nicholas C. Wolff, James A. Richardson, Merrill Egorin, Robert L. Ilaria, Jr

Blood (2003) 101 (12): 5010–5013.

https://doi.org/10.1182/blood-2002-10-3059

Published: 2003

Journal Articles

Establishment of a murine model for therapy-treated chronic myelogenous leukemia using the tyrosine kinase inhibitor STI571

Nicholas C. Wolff, Robert L. Ilaria, Jr

Blood (2001) 98 (9): 2808–2816.

https://doi.org/10.1182/blood.V98.9.2808

Published: 2001

Journal Articles

The Src homology 2 domain of Bcr/Abl is required for efficient induction of chronic myeloid leukemia–like disease in mice but not for lymphoid leukemogenesis or activation of phosphatidylinositol 3-kinase

Sergei Roumiantsev, Isabel E. de Aos, Lyuba Varticovski, Robert L. Ilaria, Richard A. Van Etten

Blood (2001) 97 (1): 4–13.

https://doi.org/10.1182/blood.V97.1.4

Published: 2001

Journal Articles

Dominant Negative Mutants Implicate STAT5 in Myeloid Cell Proliferation and Neutrophil Differentiation

Robert L. Ilaria, Jr, Robert G. Hawley, Richard A. Van Etten

Blood (1999) 93 (12): 4154–4166.

https://doi.org/10.1182/blood.V93.12.4154

Published: 1999

NARROW

STAT5 signaling is required for the efficient induction and maintenance of CML in mice

PD166326, a novel tyrosine kinase inhibitor, has greater antileukemic activity than imatinib mesylate in a murine model of chronic myeloid leukemia

STAT5 and STAT5A Signaling Play an Important Role in the Pathophysiology of the CML-Like Myeloproliferative Disorder in Mice.

The CNS is a sanctuary for leukemic cells in mice receiving imatinib mesylate for Bcr/Abl-induced leukemia

Establishment of a murine model for therapy-treated chronic myelogenous leukemia using the tyrosine kinase inhibitor STI571

The Src homology 2 domain of Bcr/Abl is required for efficient induction of chronic myeloid leukemia–like disease in mice but not for lymphoid leukemogenesis or activation of phosphatidylinositol 3-kinase

Dominant Negative Mutants Implicate STAT5 in Myeloid Cell Proliferation and Neutrophil Differentiation

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ASH Publications

American Society of Hematology

STAT5 signaling is required for the efficient induction and maintenance of CML in mice

PD166326, a novel tyrosine kinase inhibitor, has greater antileukemic activity than imatinib mesylate in a murine model of chronic myeloid leukemia

STAT5 and STAT5A Signaling Play an Important Role in the Pathophysiology of the CML-Like Myeloproliferative Disorder in Mice.

The CNS is a sanctuary for leukemic cells in mice receiving imatinib mesylate for Bcr/Abl-induced leukemia

Establishment of a murine model for therapy-treated chronic myelogenous leukemia using the tyrosine kinase inhibitor STI571

The Src homology 2 domain of Bcr/Abl is required for efficient induction of chronic myeloid leukemia–like disease in mice but not for lymphoid leukemogenesis or activation of phosphatidylinositol 3-kinase

Dominant Negative Mutants Implicate STAT5 in Myeloid Cell Proliferation and Neutrophil Differentiation

Email alerts

ASH Publications

American Society of Hematology

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