FCGR3A polymorphism : It is helpful for the management of diffuse large B-cell lymphoma

Author:

Zhong Xushu1,Xu Juan1,Yang Yunfan1,Liu Qinyu1,Tang Wenjiao1,Wang Jie1,Zhang Chunlan1,Lv Shuli1,Long Yanhong1,Xu Caigang1

Affiliation:

1. Department of Hematology, West China Hospital of Sichuan University

Abstract

Abstract

Fc receptors (FcRs) polymorphisms may affect the affinity of rituximab for antibody-dependent cellular cytotoxicity (ADCC) effector cells. The C1qA polymorphism may influence C1q levels, but their significance in treatment response and survival is unknown. This study evaluated the role of FCGR3A, C1qA, and HLA-G polymorphisms in the outcomes of patients with diffuse large B cell lymphoma (DLBCL) treated with rituximab and chemotherapy. Genomic DNA was isolated from the peripheral blood in 314 patients with newly diagnosed DLBCL. The association of polymorphisms in FCGR3A, C1qA, and HLA-G genes with overall response rate (ORR) and overall survival (OS) was analyzed. The ORR for FCGR3A genotypes VV, FV, and FF were 90.3, 82.7, and 84.7%, respectively, there was no statistical difference (P > 0.05). A significant difference was observed in the 5-year OS rate between the FF (51.8%), FV (66.9%), and VV (74.2%) genotypes (P = 0.009). The 5-year OS rate for patient with FF genotypes treated for ≤ six cycles was significantly lower than those treated for > six cycles (46 vs. 65.1%, P = 0.018). No statistically significant relationship was found between the C1qA gene polymorphism and patients' outcomes (P > 0.05). The HLA-G gene polymorphism was rarely detected in this study. FCGR3A gene polymorphism was associated with the survival of DLBCL patients and acted as an independent prognostic factor. Prolonged treatment has been anticipated to improve patients’ survival among rituximab-insensitive FF genotype patients. In contrast, more than six cycles of treatment did not result in additional survival benefits for patients with rituximab-sensitive VV and FV genotype.

Publisher

Springer Science and Business Media LLC

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