Is there any place for novel agents in treating biliary tract cancer?

Perego, Gianluca; Burgio, Valentina; Nozza, Renata; Longobardo, Giorgia; Bernecich, Marco; Luciani, Andrea; Petrelli, Fausto

doi:10.1007/s12032-021-01463-4

Cited by 1 publication

(2 citation statements)

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“…Under normal physiological conditions, the balance between co-stimulatory and co-inhibitory molecules ( 3 ) and the balance of immune checkpoint molecules, maintains the optimum immune effect of T cells ( 4 ). However, tumor cell growth can disrupt this balance, causing an abnormal upregulation of co-suppressor molecules and their related ligands, such as PD-1 and PD-L1 ( 5 ). Pardoll and his co-workers ( 6 ) showed that blocking co-inhibitory molecules from binding to ligands (blocking the PD-1/PD-L1 signaling pathway) can reverse the tumor immune microenvironment and enhance and maintain the endogenous anti-tumor effect, resulting in durable tumor control ( 7 ).…”

Section: Introductionmentioning

confidence: 99%

“…Pardoll and his co-workers ( 6 ) showed that blocking co-inhibitory molecules from binding to ligands (blocking the PD-1/PD-L1 signaling pathway) can reverse the tumor immune microenvironment and enhance and maintain the endogenous anti-tumor effect, resulting in durable tumor control ( 7 ). Therefore, immune checkpoint blocker anti-PD-1 and anti-PD-L1 antibodies have now become one of the most promising directions in antitumor therapy ( 5 , 7 – 9 ).…”

Section: Introductionmentioning

confidence: 99%

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Regulation of post-translational modification of PD-L1 and advances in tumor immunotherapy

et al. 2023

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The immune checkpoint molecules programmed cell death receptor 1 (PD-1) and programmed death ligand 1 (PD-L1) are one of the most promising targets for tumor immunotherapy. PD-L1 is overexpressed on the surface of tumor cells and inhibits T cell activation upon binding to PD⁃1 on the surface of T cells, resulting in tumor immune escape. The therapeutic strategy of targeting PD-1/PD-L1 involves blocking this binding and restoring the tumor-killing effect of immune cells. However, in clinical settings, a relatively low proportion of cancer patients have responded well to PD-1/PD-L1 blockade, and clinical outcomes have reached a bottleneck and no substantial progress has been made. In recent years, PD-L1 post-translation modifications (PTMs) have gradually become a hot topic in the field of PD-L1 research, which will provide new insights to improve the efficacy of current anti-PD-1/PD-L1 therapies. Here, we summarized and discussed multiple PTMs of PD-L1, including glycosylation, ubiquitination, phosphorylation, acetylation and palmitoylation, with a major emphasis on mechanism-based therapeutic strategies (including relevant enzymes and targets that are already in clinical use and that may become drugs in the future). We also summarized the latest research progress of PTMs of PD-L1/PD-1 in regulating immunotherapy. The review provided novel strategies and directions for tumor immunotherapy research based on the PTMs of PD-L1/PD-1.

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