The prognostic value of programmed cell death ligand 1 expression in non-Hodgkin lymphoma: a meta-analysis

程序性死亡配体1表达在非霍奇金淋巴瘤中的预后价值:一项荟萃分析

阅读:1

Abstract

OBJECTIVE: Although the prognostic value of programmed cell death-ligand 1 (PD-L1) expression in non-Hodgkin lymphoma (NHL) has been evaluated in many studies, the results remain controversial. To investigate the prognostic role of PD-L1 expression and the association between PD-L1 expression and clinicopathological features of NHL, we performed a meta-analysis. METHODS: The PubMed, EMBASE, and Cochrane Library databases were searched up to November 30, 2017. The hazard ratio (HR), 95% confidence interval (CI), and odds ratios (OR) with 95% CIs were combined to evaluate the association of PD-L1 expression with overall survival (OS) and clinicopathological features. Review manager 5.3 and STATA 12.0 were used in this meta-analysis. RESULTS: A total of 2,005 patients across nine studies were enrolled in our meta-analysis, and the pooled results showed that high PD-L1 expression was associated with a poor prognosis (HR=2.04, 95% CI: 1.18-3.54, P=0.01). In the subgroup analysis according to histology types, pooled results demonstrated that an increased PD-L1 expression was an unfavorable prognostic factor for diffuse large B-cell lymphoma (HR=1.92, 95% CI: 1.06-3.48, P=0.03) but not for natural killer/T-cell lymphoma (HR=2.41, 95% CI: 0.47-12.22, P=0.29). Pooled ORs indicated that PD-L1 expression was higher in NHL with international prognostic indices of ≥3. However, PD-L1 expression had no correlation with gender, age, disease stage, lactate dehydrogenase level, B symptoms, and germinal center B-cell-like lymphoma. CONCLUSIONS: High PD-L1 expression was a poor prognostic biomarker in patients with NHL. Because of our limited sample size, high-quality studies with larger sample sizes are needed to validate our results.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。