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Journal Articles

Jak2 Phosphorylates Tyr 177 of Bcr-Abl Activating the Ras and PI-3 Kinase Pathways and Maintains Functional Levels of Bcr-Abl in Chronic Myelogenous Leukemia.

Ajoy K. Samanta, PhD, Sandip N. Chakraborty, Xiaoping Sun, M.D., Ph.D, Ellen Schlette, M.D., Waldemar Priebe, Ph.D., Ralph B. Arlinghaus, PhD

Blood (2009) 114 (22): 39.

https://doi.org/10.1182/blood.V114.22.39.39

Published: 2009

Journal Articles

Disruption of the Bcr-Abl/Jak2/HSP90 Network Complex Leading to Induction of Apoptosis in Drug-Resistant CML Cells by a New Compound WP1193

Ajoy K. Samanta, PhD, Sandip N. Chakraborty, Susmita Samanta, Ph.D., Yan Wang, M.D., Xiaoping Sun, MD, PhD, E. Schlette, Waldemar Priebe, Ph.D., Ralph B. Arlinghaus, PhD

Blood (2008) 112 (11): 3199.

https://doi.org/10.1182/blood.V112.11.3199.3199

Published: 2008

Journal Articles

Jak2 Regulates Lyn Tyrosine Kinase through Interference with the SET/PP2A/Shp1 Pathway and Inhibition of Jak2 Induced Apoptosis in BCR-ABL+ Imatinib-Sensitive and Resistant CML Cells.

Ajoy K. Samanta, PhD, Sandip Chakravorty, MS, Yan Wang, MD, Jorge Cortes, MD, Hagop Kantarjian, MD, Richard E. Champlin, MD, Danilo Perrotti, MD, PhD, Ralph B. Arlinghaus, PhD

Blood (2007) 110 (11): 3342.

https://doi.org/10.1182/blood.V110.11.3342.3342

Published: 2007

Journal Articles

Oncogenic Transformation of NIH 3T3 Fibroblasts by BCR-ABL Oncoprotein Requires the IL-3 Receptor.

Wenjing Tao, PhD, Hui Lin, MD, Tong Sun, MS, Ajoy K. Samanta, PhD, Ralph B. Arlinghaus, PhD

Blood (2007) 110 (11): 3370.

https://doi.org/10.1182/blood.V110.11.3370.3370

Published: 2007

Journal Articles

Jak2: A Potential Therapeutic Target for Chronic Myelogenous Leukemia (CML).

Ajoy K. Samanta, PhD, Hui Lin, M.D., Tong Sun, M.S., Hagop Kantarjian, M.D., Ralph B. Arlinghaus, Ph.D.

Blood (2006) 108 (11): 2121.

https://doi.org/10.1182/blood.V108.11.2121.2121

Published: 2006

NARROW

Jak2 Phosphorylates Tyr 177 of Bcr-Abl Activating the Ras and PI-3 Kinase Pathways and Maintains Functional Levels of Bcr-Abl in Chronic Myelogenous Leukemia.

Disruption of the Bcr-Abl/Jak2/HSP90 Network Complex Leading to Induction of Apoptosis in Drug-Resistant CML Cells by a New Compound WP1193

Jak2 Regulates Lyn Tyrosine Kinase through Interference with the SET/PP2A/Shp1 Pathway and Inhibition of Jak2 Induced Apoptosis in BCR-ABL+ Imatinib-Sensitive and Resistant CML Cells.

Oncogenic Transformation of NIH 3T3 Fibroblasts by BCR-ABL Oncoprotein Requires the IL-3 Receptor.

Jak2: A Potential Therapeutic Target for Chronic Myelogenous Leukemia (CML).

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ASH Publications

American Society of Hematology

Jak2 Phosphorylates Tyr 177 of Bcr-Abl Activating the Ras and PI-3 Kinase Pathways and Maintains Functional Levels of Bcr-Abl in Chronic Myelogenous Leukemia.

Disruption of the Bcr-Abl/Jak2/HSP90 Network Complex Leading to Induction of Apoptosis in Drug-Resistant CML Cells by a New Compound WP1193

Jak2 Regulates Lyn Tyrosine Kinase through Interference with the SET/PP2A/Shp1 Pathway and Inhibition of Jak2 Induced Apoptosis in BCR-ABL+ Imatinib-Sensitive and Resistant CML Cells.

Oncogenic Transformation of NIH 3T3 Fibroblasts by BCR-ABL Oncoprotein Requires the IL-3 Receptor.

Jak2: A Potential Therapeutic Target for Chronic Myelogenous Leukemia (CML).

Email alerts

ASH Publications

American Society of Hematology

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