Abstract
Background:DLBCL is the most common subtype of non‐Hodgkin's lymphomas. However, the pathogenesis of DLBCL is not fully understood. Transcription factors or signaling pathways involved in normal B cell development and function might represent future therapeutic targets. Such a transcription factor is MEF2 C contributing to B cell activation and germinal center formation.Aims:This study aims at investigating the role of MEF2 C as prognostic biomarker in DLBCL.Methods82 patients with DLBCL were enrolled in our study. We assessed the expression of MEF2 C by performing immunohistochemistry (IHC) on paraffin slides of 62 tissue blocks and results were evaluated by using the H‐score semiquantitative approach, with a range from 0 to 300. Additionally, we analyzed clinical [sex, age, stage of DLBCL, performance status, extranodal sites, B symptoms, International Prognostic Index (IPI), age‐adjusted IPI, revised‐IPI, National Comprehensive Cancer Network (NCCN)‐IPI], laboratory [lactate dehydrogenase (LDH), hemoglobin (Hb), white blood cells (WBC), neutrophils, lymphocytes, monocytes, platelets and beta‐2‐microglobulin] and pathologic characteristics (CD10, BCL6, MUM‐1, Ki‐67) of patients in relation to overall (OS) and disease free survival (DFS).Results:Mean and median value of MEF2 C H‐score was 120 ± 58. We observed a statistical significant correlation with age (p= 0.021) and a tendency to correlate with LDH (p = 0.18). The expression of MEF2 C was not associated with other clinical or laboratory values. MEF2 C positivity >80% was correlated with borderline inferior OS (p = 0.083). Among patients, who survived more than 12 months after initial diagnosis, those with MEF2 C H score <120 had a significant better OS comparing with those with MEF2 C H score >120 (p = 0.009).Summary/Conclusion:High IHC expression of MEF2 C showed a negative prognostic influence in patients with OS more than 12 months after initial diagnosis. However, these results should be confirmed in larger groups of DLBCL patients and the underlying oncogenic mechanism of MEF2 C in DLBCL should be further explored.
Published Version
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