@article{784ddff9120545bfb4258518b1e04dba,
title = "Plasma soluble programmed death ligand 1 levels predict clinical response in peripheral T-cell lymphomas",
abstract = "Immune checkpoints, including PD-1/PD-L1, play an important role in immunosuppression in various malignancies. Elevated levels of soluble programmed death ligand 1 (sPD-L1) are associated with worse prognosis in multiple myeloma and diffuse large B cell lymphoma. Herein, the purpose of this study is to investigate the relationships between plasma sPD-L1 levels and clinical response in peripheral T-cell lymphoma (PTCL) patients. A total of 37 PTCL patients and 20 healthy volunteers were enrolled. Peripheral blood from patients was collected prior to systemic therapy. Plasma levels of sPD-L1 and IFN-γ were measured by enzyme-linked immunosorbent assay (ELISA). PD-L1 expression in tissues was detected by immunohistochemistry (IHC). Clinical response for patients was evaluated. ONCOMINE database analyses showed that PD-L1 mRNA expression was significantly upregulated in PTCLs. The median sPD-L1 level was 0.729 ng/mL for 20 healthy volunteers and 1.696 ng/mL for 37 PTCL patients which was significantly higher than that in healthy volunteers (0.000). The sPD-L1 level was positively correlated with IFN-γ level (0.000, r = 0.849) and was also positively associated with clinical staging (0.045), LDH level (0.003), and β2-MG level (0.045). Patients with high sPD-L1 level had lower overall response rate than those with low sPD-L1 level (88.9% vs 50.0%, 0.022) and tended to have poorer PFS and OS. PD-L1 expression in tissues matched very well with the sPD-L1 level in PTCL patients. In conclusion, PTCL patients had higher sPD-L1 level compared with healthy volunteers. High sPD-L1 level was correlated with worse clinical response, suggesting that sPD-L1 level was an underlying plasma biomarker to predict the prognosis for PTCL patients.",
keywords = "IFN-γ, PTCLs, clinical response, sPD-L1",
author = "Xuhan Zhang and Lu Liu and Shiyong Zhou and Kuo Zhao and Zheng Song and Ge Hu and Tingting Zhang and Yang Li and Lihua Qiu and Lanfang Li and Zhengzi Qian and Bin Meng and Yi Pan and Xiubao Ren and Xianhuo Wang and Huilai Zhang and Kai Fu",
note = "Funding Information: Key Research Projects of Tianjin Municipal Health Bureau, Grant/Award Numbers: 15KG145 and 2015KZ081; National Key New Drug Creation Special Programs, Grant/Award Number: 2017ZX09304‐021, 2018ZX09201015; National Natural Science Foundation of China, Grant/Award Number: 81770213; National Human Genetic Resources Sharing Service Platform, Grant/ Award Number: 2005DKA21300; Tianjin Medical University Cancer Institute and Hospital Foundation, Grant/Award Number: 1504 Funding Information: This study was supported by the National Natural Science Foundation of China (81770213), the National Key New Drug Creation Special Programs (2017ZX09304-021, 2018ZX09201015), the Key Research Projects of Tianjin Municipal Health Bureau (15KG145, 2015KZ081), the Tianjin Medical University Cancer Institute and Hospital Foundation (1504), and the National Human Genetic Resources Sharing Service Platform (2005DKA21300)/Cancer Biobank of Tianjin Medical University Cancer Institute and Hospital. Funding Information: This study was supported by the National Natural Science Foundation of China (81770213), the National Key New Drug Creation Special Programs (2017ZX09304‐021, 2018ZX09201015), the Key Research Projects of Tianjin Municipal Health Bureau (15KG145, 2015KZ081), the Tianjin Medical University Cancer Institute and Hospital Foundation (1504), and the National Human Genetic Resources Sharing Service Platform (2005DKA21300)/Cancer Biobank of Tianjin Medical University Cancer Institute and Hospital. Publisher Copyright: {\textcopyright} 2019 The Authors. Hematological Oncology Published by John Wiley & Sons Ltd",
year = "2019",
month = aug,
doi = "10.1002/hon.2636",
language = "English (US)",
volume = "37",
pages = "270--276",
journal = "Hematological Oncology",
issn = "0278-0232",
publisher = "John Wiley and Sons Ltd",
number = "3",
}