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Journal Articles

Rituximab infusion induces NK activation in lymphoma patients with the high-affinity CD16 polymorphism

Suresh Veeramani, Siao-Yi Wang, Christopher Dahle, Sue Blackwell, Laura Jacobus, Tina Knutson, Anna Button, Brian K. Link, George J. Weiner

Blood (2011) 118 (12): 3347–3349.

https://doi.org/10.1182/blood-2011-05-351411

Published: 2011

Includes: Supplemental data

Journal Articles

Depletion of the C3 component of complement enhances the ability of rituximab-coated target cells to activate human NK cells and improves the efficacy of monoclonal antibody therapy in an in vivo model

Siao-Yi Wang, Suresh Veeramani, Emilian Racila, Jeffrey Cagley, David C. Fritzinger, Carl-Wilhelm Vogel, William St John, George J. Weiner

Blood (2009) 114 (26): 5322–5330.

https://doi.org/10.1182/blood-2009-01-200469

Published: 2009

Journal Articles

Rituximab Infusion Induces NK Activation in Subjects with the High Affinity CD16 Polymorphism.

George J Weiner, MD, Suresh Veeramani, Siao-Yi Wang, Christopher Dahle, Sue Blackwell, Laura Jacobus, Tina Knutson, Allison C Knutson, Brian J Smith, Brian K Link, MD

Blood (2009) 114 (22): 1705.

https://doi.org/10.1182/blood.V114.22.1705.1705

Published: 2009

Journal Articles

Depletion of the C3 Component of Complement Enhances the Ability of Rituximab-Coated Target Cells to Activate Human NK Cells and Improves the Efficacy of Monoclonal Antibody Therapy in An in Vivo Model

Siao- Yi Wang, Jeffrey Cagley, David Fritzinger, Carl-Wilhelm Vogel, William St. John, George J Weiner

Blood (2008) 112 (11): 3620.

https://doi.org/10.1182/blood.V112.11.3620.3620

Published: 2008

Journal Articles

NK-cell activation and antibody-dependent cellular cytotoxicity induced by rituximab-coated target cells is inhibited by the C3b component of complement

Siao-Yi Wang, Emilian Racila, Ronald P. Taylor, George J. Weiner

Blood (2008) 111 (3): 1456–1463.

https://doi.org/10.1182/blood-2007-02-074716

Published: 2008

Journal Articles

The C3b Component of Complement Inhibits NK Cell Activation Induced by Rituximab-Coated Target Cells.

Siao-Yi Wang, BA, Emilian Racila, MD, Ronald P. Taylor, PhD, George J. Weiner, MD

Blood (2006) 108 (11): 2505.

https://doi.org/10.1182/blood.V108.11.2505.2505

Published: 2006

Journal Articles

Anti-CD20 monoclonal antibody with enhanced affinity for CD16 activates NK cells at lower concentrations and more effectively than rituximab

Julie A. Bowles, Siao-Yi Wang, Brian K. Link, Barrett Allan, Gregory Beuerlein, Mary-Ann Campbell, David Marquis, Brian Ondek, James E. Wooldridge, Brian J. Smith, James B. Breitmeyer, George J. Weiner

Blood (2006) 108 (8): 2648–2654.

https://doi.org/10.1182/blood-2006-04-020057

Published: 2006

NARROW

Rituximab infusion induces NK activation in lymphoma patients with the high-affinity CD16 polymorphism

Depletion of the C3 component of complement enhances the ability of rituximab-coated target cells to activate human NK cells and improves the efficacy of monoclonal antibody therapy in an in vivo model

Rituximab Infusion Induces NK Activation in Subjects with the High Affinity CD16 Polymorphism.

Depletion of the C3 Component of Complement Enhances the Ability of Rituximab-Coated Target Cells to Activate Human NK Cells and Improves the Efficacy of Monoclonal Antibody Therapy in An in Vivo Model

NK-cell activation and antibody-dependent cellular cytotoxicity induced by rituximab-coated target cells is inhibited by the C3b component of complement

The C3b Component of Complement Inhibits NK Cell Activation Induced by Rituximab-Coated Target Cells.

Anti-CD20 monoclonal antibody with enhanced affinity for CD16 activates NK cells at lower concentrations and more effectively than rituximab

Email alerts

ASH Publications

American Society of Hematology

Rituximab infusion induces NK activation in lymphoma patients with the high-affinity CD16 polymorphism

Depletion of the C3 component of complement enhances the ability of rituximab-coated target cells to activate human NK cells and improves the efficacy of monoclonal antibody therapy in an in vivo model

Rituximab Infusion Induces NK Activation in Subjects with the High Affinity CD16 Polymorphism.

Depletion of the C3 Component of Complement Enhances the Ability of Rituximab-Coated Target Cells to Activate Human NK Cells and Improves the Efficacy of Monoclonal Antibody Therapy in An in Vivo Model

NK-cell activation and antibody-dependent cellular cytotoxicity induced by rituximab-coated target cells is inhibited by the C3b component of complement

The C3b Component of Complement Inhibits NK Cell Activation Induced by Rituximab-Coated Target Cells.

Anti-CD20 monoclonal antibody with enhanced affinity for CD16 activates NK cells at lower concentrations and more effectively than rituximab

Email alerts

ASH Publications

American Society of Hematology

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