3 results match your criteria: "P.R. China. cai.jiabin@zs-hospital.sh.cn.[Affiliation]"

N-linked glycosylation of PD-L1/PD-1: an emerging target for cancer diagnosis and treatment.

J Transl Med

July 2024

Department of Liver Surgery and Transplantation, Zhongshan Hospital, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Liver Cancer Institute, Fudan University, Shanghai, 200032, P.R. China.

During tumorigenesis and progression, the immune checkpoint programmed death-1 (PD-1) and its ligand programmed death ligand-1 (PD-L1) play critical roles in suppressing T cell-mediated anticancer immune responses, leading to T-cell exhaustion and subsequent tumor evasion. Therefore, anti-PD-L1/PD-1 therapy has been an attractive strategy for treating cancer over the past decade. However, the overall efficacy of this approach remains suboptimal, revealing an urgent need for novel insights.

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PKCα/ZFP64/CSF1 axis resets the tumor microenvironment and fuels anti-PD1 resistance in hepatocellular carcinoma.

J Hepatol

July 2022

Department of Liver Surgery and Transplantation, Key Laboratory of Carcinogenesis and Cancer Invasion (Ministry of Education), Liver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai, 200032, P. R. China. Electronic address:

Background & Aims: Despite remarkable advances in treatment, most patients with hepatocellular carcinoma (HCC) respond poorly to anti-programmed cell death 1 (anti-PD1) therapy. A deeper insight into the tolerance mechanism of HCC against this therapy is urgently needed.

Methods: We performed next-generation sequencing, multiplex immunofluorescence, and dual-color immunohistochemistry and constructed an orthotopic HCC xenograft tumor model to identify the key gene associated with anti-PD1 tolerance.

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Article Synopsis
  • Natural killer (NK) cells are important for fighting tumors, but their dysfunction is observed in hepatocellular carcinoma (HCC), which is not fully understood.
  • The study found that the circular RNA circUHRF1 is expressed at higher levels in HCC tissues and correlates with poor prognosis and NK cell dysfunction by reducing their ability to secrete key immune signals.
  • CircUHRF1 also contributes to NK cell dysfunction by promoting TIM-3 expression through miR-449c-5p degradation, potentially leading to resistance against immunotherapy in HCC patients.
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