Polymorphisms in FcγRIIIA (CD16) receptor expression are associated with clinical response to rituximab in Waldenstrom's macroglobulinemia.

@article{Treon2004PolymorphismsIF,
  title={Polymorphisms in Fc$\gamma$RIIIA (CD16) receptor expression are associated with clinical response to rituximab in Waldenstrom's macroglobulinemia.},
  author={Steven P P Treon and Mark Hansen and Andrew R. Branagan and Christos E. Emmanouilides and Eva Kimby and Stanley R. Frankel and Nikolaos Touroutoglou and David G. Maloney and Kenneth C. Anderson and Edward A. Fox},
  journal={Journal of clinical oncology : official journal of the American Society of Clinical Oncology},
  year={2004},
  volume={22 14\_suppl},
  pages={6556}
}
  • S. TreonM. Hansen E. Fox
  • Published 15 July 2004
  • Medicine, Biology
  • Journal of clinical oncology : official journal of the American Society of Clinical Oncology
6556 Background: Polymorphisms in FcγRIIIA (CD16) receptor expression modulate human IgG1 binding, and antibody dependent cell mediated cytotoxicity, and may therefore impact responses to rituximab in patients with WM. METHODS We therefore performed sequencing of all DNA coding regions for FcγRIIIA in 58 patients with Waldenstrom's macroglobulinemia (WM) treated with rituximab. Two distinct, but linked polymorphisms (FcγRIIIA-48 and -158) were commonly observed. All patients with FcγRIIIA… 
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The results of these studies demonstrate that there is wide linkage within and between polymorphisms in FcγRIIa and F cγRIIIa and might provide an explanation for why polymorphisms at Fc εIIa are associated with rituximab responses despite a lack of impact on IgG1 binding.

The impact of FcγRIIa and FcγRIIIa gene polymorphisms on responses to RCHOP chemotherapy in diffuse large B-cell lymphoma patients

The findings of the present study indicate that FcγR polymorphisms have no influence on the survival of DLBCL patients.

The impact of Fc-γ receptor polymorphisms in elderly patients with diffuse large B-cell lymphoma treated with CHOP with or without rituximab.

The interaction of R-CHOP, but not CHOP with FcγRIIIa polymorphisms, indicates a window of opportunity for CD20 antibodies designed to mediate enhanced antibody-dependent cellular cytotoxicity.

The loss of the CD16 B73.1/Leu11c epitope occurring in some primary immunodeficiency diseases is not associated with the FcgammaRIIIa-48L/R/H polymorphism.

It is suggested that the loss of the B73.1/Leu11c binding epitope is connected with primary immunodeficiency disorders, but not associated with the FcgammaRIIIa-48 polymorphism.

FCGR3A gene polymorphisms may correlate with response to frontline R-CHOP therapy for diffuse large B-cell lymphoma.

The FCGR3A single nucleotide polymorphism (SNP) is predictive of response to R-CHOP, but does not correlate with survival in patients with DLBCL, and FcR polymorphism can affect rituximab's affinity for ADCC effector cells.

FCGR2C genotyping by pyrosequencing reveals linkage disequilibrium with FCGR3A V158F and FCGR2A H131R polymorphisms in a Caucasian population

A strong and a weaker linkage disequilibrium associating the FCGR2C-ORF allele with the FC GR3A-158V and the FC2A-131H allele, respectively are demonstrated.

Increased natural killer cell expression of CD16, augmented binding and ADCC activity to rituximab among individuals expressing the Fc{gamma}RIIIa-158 V/V and V/F polymorphism.

Results suggest that individuals expressing at least one valine at FcgammaRIIIa-158 might, in part, have better clinical outcomes due to increased CD16 expression, rituximab binding, and ritUXimab-mediated, antibody-dependent cellular cytotoxicity (ADCC).

The 158VV Fcgamma receptor 3A genotype is associated with response to rituximab in rheumatoid arthritis: results of an Italian multicentre study

The 158VV FCGR3A genotype was associated with response to RTX in a large cohort of RA patients and may be helpful to plan RTX treatment, and May be integrated with clinical predictors.

Immunoglobulin G Fc receptor FcgammaRIIIa 158 V/F polymorphism correlates with rituximab-induced neutropenia after autologous transplantation in patients with non-Hodgkin's lymphoma.

The high affinity FcgammaRIIIa 158 V allele is associated with rituximab-induced neutropenia after autologous transplantation and is a potential tool to identify a high-risk population for developing neutropania after antibody therapy.

Flow cytometric assay for determination of FcγRIIIA-158 V/F polymorphism

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