PB1800 PROGNOSTIC RELEVANCE OF PROTEIN EXPRESSION, CLINICAL FACTORS, AND MYD88 MUTATION IN PRIMARY TESTICULAR DIFFUSE LARGE B‐CELL LYMPHOMA

Abstract

Background:Primary testicular diffuse large B‐cell lymphoma (tDLBCL) is a rare, clinically aggressive form of extranodal lymphoma confined to the testis. It is known to have a poor prognosis, with an outcome inferior to nodal DLBCL. Only a few studies of tDLBCL have included immunohistochemical and molecular investigations, and little is known about the prognostic significance of the in situ tissue antigen expression profiles in tDLBCL.Aims:We performed a mutation analysis of the MYD88 L265P mutation in 17 tDLBCL patients and investigated the immunophenotypic biomarkers and clinicopathological factors associated with tDLBCL.Methods:Clinical date and paraffin‐embedded material from 17 patients presenting with tDLBCL were retrieved from the archives of the pathology department at the Nanjing Drum Tower Hospital.Immunohistochemistry was used to examine the expression of CD10, Bcl2, Bcl6, MUM1, C‐myc, P50, P65, P53, PSTAT3, OCT4, PIM1, CXCR4 and JAK2. MYD88 gene mutation analysis and complete clinical data evaluation were carried out and linked to overall survival time.Results:High expression of B‐cell lymphoma 2 was detected in 7/17 tDLBCL patients and was associated with a poor prognosis in a univariate model. Most of these patients (6/7) also expressed c‐myc. P50, JAK2, PSTAT3, PIM1 and CXCR4 were also upregulated in tDLBCLs. There were seventeen cases of tDLBCL; in total, 82.4% (14/17) of patients exhibited an activated B‐cell‐like phenotype (ABC), 56.3% (9/16) of patients harbored the MYD88 L265P mutation and showed a correlation between the MYD88 L265P mutation and the ABC phenotype (p = 0.009). However, there was no association between the MYD88 mutation status and overall survival.Summary/Conclusion:We demonstrated that clinical factors such as age, IPI score, stage, lack of B symptoms and the over‐expression of Bcl‐2 are independent prognostic factors determining overall survival and that the over‐expression of P50, JAK2, PSTAT3, PIM1 and CXCR4 may promote the pathogenesis of tDLBCL. Moreover, we found a high prevalence of the MYD88 L265P mutation in tDLBCL, which may reflect a fairly consistent genetic feature in tDLBCL.