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

OpenAlex İngilizce

BACKGROUND: 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. 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. DISCUSSION: 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.