Abstract
The precise clinicopathologic significance of myeloid differentiation primary response gene (MYD88) L265P mutation in diffuse large B-cell lymphomas (DLBCLs) remains elusive. To investigate the frequency and clinicopathologic significance of the MYD88 L265P mutation in DLBCLs, we conducted a meta-analysis of 40 published studies on 2736 DLBCL patients. We collected relevant published research findings identified using the PubMed and Embase databases. The effect sizes of outcome parameters were calculated using a random-effects model. In this meta-analysis, the MYD88 L265P mutation in DLBCL showed a significant difference according to tumor sites. The overall incidence of the MYD88 L265P mutation in DLBCLs, excluding the central nervous system and testicular DLBCLs, was 16.5%. Notably, the MYD88 L265P mutation rates of CNS and testicular DLBCL patients were 60% and 77%, respectively. Interestingly, the MYD88 L265P mutation was more frequently detected in activated B-cell-like (ABC) or non-germinal center B-cell-like (GCB) than GCB subtype (OR = 3.414, p < 0.001). The MYD88 L265P mutation was significantly associated with old age and poor overall survival, but not with sex and clinical stage. This pooled analysis demonstrates that the MYD88 L265P mutation is significantly associated with the tumor sites and molecular subtypes in DLBCL patients.
Highlights
Myeloid differentiation primary response gene (MYD88) is an adaptor protein that activates the nuclear transcription factor κB (NF-κB) signaling through most of the Toll-like receptors (TLRs)[1]
Twenty-nine studies have reported that the frequency of MYD88 L265P mutation in 2285 diffuse large B-cell lymphomas (DLBCLs) patients except for central nervous system (CNS) and testicular lymphomas was 16.5%2, 3, 6, 7, 9–11, 13, 16–22, 24, 25, 27, 28, 30, 31, 33–39, 41
In the funnel plot and Egger regression test, there was no evidence of publication bias except for the meta-analysis for the association of MYD88 L265P mutation with the DLBCL subtypes (Supplementary Table S3) (Fig. 5). This pooled analysis showed that the tumor location of origin in DLBCL contributes to the prevalence difference of MYD88 L265P mutation
Summary
Myeloid differentiation primary response gene (MYD88) is an adaptor protein that activates the nuclear transcription factor κB (NF-κB) signaling through most of the Toll-like receptors (TLRs)[1]. Many investigators have reported that the prevalence of MYD88 L265P mutation ranges from 0% to 94% in different series of diffuse large B-cell lymphoma (DLBCL) patients[2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41]. Several studies have suggested that the frequency of MYD88 L265P mutation may vary depending on the tumor site or molecular subtype of DLBCL2, 8, 21, 24, 30, 41, but individual studies with different designs hinder clear conclusions. The clinicopathologic significance of the MYD88 L265P mutation in each DLBCL patient was controversial.
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