LAUSR

Meier survival curve analyses with log‐rank test, univariate and multivariate Cox regression model analyses of overall survival (OS), and progression‐free survival (PFS) were performed. Gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) analysis in whole‐genome profiling were conduct to predict potential functions of MELK in DLBCL. Results: Markedly increased expression of MELK in DLBCL tissues (9.299 ± 0.081, n = 89) compared with B cells from normal tonsil tissues (7.218 ± 0.243, n = 33) were observed (Figure A). Furthermore, in the cohort of 471 DLBCL patients with R‐CHOP treatment, stratified high MELK expression is closely associated with advanced Ann Arbor stage (P = .026), high IPI score (P = .036), activated B‐cell– like (ABC) DLBCL subtype (P = .013), and patients' non‐CR rates (P = .001). Kaplan‐Meier survival curve analyses indicated MELK overexpression was of significant correlation with inferior OS (P = .001) and PFS (P = .018) (Figure B, C). Multivariate Cox regression analysis adjusting for validated significant parameters in univariate analysis confirmed independent prognostic value of MELK in OS of DLBCL patients (HR: 1.600; 95% CI, 1.096‐2.335, P = .015). Functional enrichment assays indicate that MELK is tightly associated with biological processes including cell division, apoptosis process and cell cycle. Besides, MELK might contribute to cancer progression of DLBCL via regulating PI3K/Akt, Ras, and p53 signaling pathways. Conclusions: We identify that MELK is an independent prognostic marker in DLBCL patients with R‐CHOP regimen. Further prospective validation are warranted to stratify patients groups with DLBCL, thus formulating individual therapeutic strategies and improving patients' survival.