{Reference Type}: Systematic Review
{Title}: The Prognostic Significance of CD79B Mutation in Diffuse Large B-Cell Lymphoma: A Meta-analysis and Systematic Literature Review.
{Author}: Xu PP;Shen R;Shi ZY;Cheng S;Wang L;Liu Y;Zhang L;Huang R;Ma X;Wu X;Yao H;Yu Y;Zhao WL;
{Journal}: Clin Lymphoma Myeloma Leuk
{Volume}: 22
{Issue}: 12
{Year}: 12 2022
{Factor}: 2.822
{DOI}: 10.1016/j.clml.2022.08.006
{Abstract}: Previous studies have shown that diffuse large B-cell lymphoma (DLBCL) subtype with both B-cell antigen receptor complex-associated protein beta chain (CD79B) and myeloid differentiation primary response 88 mutations (MYD88) had inferior outcome under standard immunochemotherapy. However, the prognostic significance of CD79B alone in DLBCL has not been fully elucidated. We conducted a meta-analysis to investigate the role of CD79B mutation on overall survival (OS) in patients with DLBCL.
We performed literature search in PubMed and Embase databases and followed PRISMA guidelines to select publications for analysis. The primary and secondary outcome was OS and progression-free survival (PFS) respectively. Hazard ratio (HR) for OS/PFS in CD79B mutant group with that in wild-type group in R-chemotherapy patients was either estimated using Cox proportional hazard model from the studies with individual participant level data or extracted from the original publication with aggregated results.
Nine eligible studies with survival information according to CD79B mutation status were included in this meta-analysis. The pooled hazard ratio for OS was 1.38 (95% CI, 1.13-1.70; p = 0.0021) for CD79B mutation, providing evidence that CD79B mutation was unfavorable prognostic factor for survival in DLBCL patients treated with immunochemotherapy. We identified the inferior prognostic impact of CD79B mutation was independent from well-established prognostic model in DLBCL, International Prognostic Index. The predictive power of CD79B mutation was stronger than that of MYD88 mutation.
This meta-analysis revealed that CD79B mutation could be a key biomarker for DLBCL disease progression and future mechanism-based target therapy in DLBCL needs to be studied.