PD-L1 and EBV LMP1 expressions in classic Hodgkin lymphomas and its correlation with clinicopathological parameters and prognosis

BACKGROUND/AIM: Programmed death pathway leads to T cell anergy. Wide range of malignancies take advantage of this pathway by programmed death-ligand 1 (PD-L1) expression either on neoplastic cells or on the nonneoplastic cells of tumour microenvironment. New therapeutic approaches have been directed against this pathway. We studied PD-L1 expression on both neoplastic Hodgkin and Reed–Sternberg (HRS) cells and cells of tumour microenvironment in classic Hodgkin lymphoma (CHL) patients and compared it with Ebstein–Barr virus (EBV) positivity, clinical data, and survival rates. MATERIALS AND METHODS: Lymph node excision materials of 56 CHL patients diagnosed between 2007 and 2017 were included in this retrospective study. PD-L1 expression of HRS cells and tumour microenvironment cells were evaluated by immunohistochemical assay. Staining intensity and rate of the PD-L1 expressions were estimated. EBV was examined by immunohistochemistry for latent membrane protein 1 (LMP1) antibody. Clinical data of 39 patients and survival data of 34 patients were compared with PD-L1 expressions on tumour cells. RESULTS: PD-L1 expression was present in HRS cells in 89.2% of the cases. There was more than 20% of PD-L1 expression in cells of tumour microenvironment in all the cases. PD-L1 positivity did not show statistically significant difference according to EBV expression, clinical parameters, and prognosis. CONCLUSION: Previous studies showed inconsistent rates for PD-L1 prevalence (20%–95.7%) in CHL patients due to differences in the study methods. Although high prevalence of PD-L1 positivity was found in majority of them, there was no statistically significant difference between PD-L1 positivity on HRS cells and EBV expression, clinical parameters, and prognosis. This high prevalence in patients with various clinical properties makes PD-L1 a potential target for new emerging immunotherapies for CHL.