PRDM1 levels are associated with clinical diseases in chronic HBV infection and survival of patients with HBV-related hepatocellular carcinoma.

Abstract:

:PR domain zinc finger protein 1 (PRDM1)/B lymphocyte-induced maturation protein 1 (BLIMP1) is a transcriptional repressor involved in B and T cell responses which are implicated in chronic hepatitis B virus (HBV) infection and hepatocellular carcinoma (HCC). This study investigated the association of PRDM1 with clinical diseases of chronic HBV infection and prognosis of HBV -related HCC patients. Serum PRDM1 levels were determined in 403 patients with chronic HBV infection (171 chronic hepatitis, 119 cirrhosis and 113 HCC), 70 HBV infection resolvers and 96 healthy control individuals. The PRDM1 levels were analyzed with regard to clinical diseases and overall survival of HCC patients. Serum PRDM1 concentrations in patients with chronic HBV infection were significantly elevated compared with infection resolvers and healthy controls. HBV-related HCC patients had the most significantly elevated PRDM1 levels. PRDM1 levels could considerably differentiate HCC from chronic hepatitis [area under receiver operating characteristic curve (AUC) 0.889, p < 0.001] or cirrhosis (AUC 0.910, p < 0.001). HCC patients with high PRDM1 levels had a poor prognosis (>300 pg/mL vs. ≤300 pg/mL, p = 0.001). High PRDM1 levels were independently associated with increased mortality in HCC patients (hazard ratio 2.997, 95% confidence interval 1.103-4.722, p = 0.003). Overall, this study demonstrated that PRDM1 levels are associated with the clinical diseases of chronic HBV infection. Highly elevated PRDM1 levels are discriminative of HCC from other clinical diseases and indicative of a poor prognosis of HCC patients. The potential association of PRDM1 levels with disease progression and treatment response warrants further investigation.

journal_name

Int Immunopharmacol

authors

Li N,Fan X,Wang X,Deng H,Zhang K,Zhang X,Wang Y,Han Q,Lv Y,Liu Z

doi

10.1016/j.intimp.2019.05.012

subject

Has Abstract

pub_date

2019-08-01 00:00:00

pages

156-162

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(19)30454-0

journal_volume

73

pub_type

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