Evidence map›Paper›PMID 38762484›Full record

ReviewMolecular cancer2024

Regulatory mechanisms of PD-1/PD-L1 in cancers.

Xin Lin, Kuan Kang, Pan Chen, Zhaoyang Zeng, Guiyuan Li, Wei Xiong, Mei Yi, Bo Xiang

Registry-linked trialAbstract readReview
In one paragraph

Review in Molecular cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07515313 (Expression of CD274), which is not on this map. Cited by 552 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
552citing papers in PubMed, 4 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT07515313 not yet recruitingnot on this mapstarted 2026, after this paper: background citation

Expression of CD274 (PD-L1) and CD276 in B-cell Malignancies: A Study by Flowcyometry

TypeobservationalSponsorAssiut UniversityRan2026 to 2030Enrolled159ConditionsB-cell Malignancies
3 · Its place in the literature

Who cites it

552 citing papers in PubMed, 4 syntheses or guidelines pooled it.

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  15. Supramolecular Degraders: An Emerging Paradigm in Targeted Protein Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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492 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Xin LinNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410013, Hunan, China.
Kuan KangNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410013, Hunan, China.
Pan ChenNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410013, Hunan, China.
Zhaoyang ZengNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410013, Hunan, China.
Guiyuan LiNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410013, Hunan, China.
Wei XiongNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410013, Hunan, China.
Mei YiDepartment of Dermotology, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China. yi_mei@csu.edu.cn.
Bo XiangNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410013, Hunan, China. xiangbolin@csu.edu.cn.

Funding

the Beijing Xisike Clinical Oncology Research Foundation Y-HR2020ZD-0052the Hunan Provincial Key Research and Development Program 2022SK2026the Independent Exploration and Innovation Program of Central South University 1053320221155the National "111" Project #111-2-12The National Natural Science Foundation of China U23A20456, 82272631, 82072596, 82173339the Natural Science Foundation of Hunan Province 2024JJ3036the scientific research program of FuRong laboratory 2023SK2094
6 · The paper itself

Abstract

Immune evasion contributes to cancer growth and progression. Cancer cells have the ability to activate different immune checkpoint pathways that harbor immunosuppressive functions. The programmed death protein 1 (PD-1) and programmed cell death ligands (PD-Ls) are considered to be the major immune checkpoint molecules. The interaction of PD-1 and PD-L1 negatively regulates adaptive immune response mainly by inhibiting the activity of effector T cells while enhancing the function of immunosuppressive regulatory T cells (Tregs), largely contributing to the maintenance of immune homeostasis that prevents dysregulated immunity and harmful immune responses. However, cancer cells exploit the PD-1/PD-L1 axis to cause immune escape in cancer development and progression. Blockade of PD-1/PD-L1 by neutralizing antibodies restores T cells activity and enhances anti-tumor immunity, achieving remarkable success in cancer therapy. Therefore, the regulatory mechanisms of PD-1/PD-L1 in cancers have attracted an increasing attention. This article aims to provide a comprehensive review of the roles of the PD-1/PD-L1 signaling in human autoimmune diseases and cancers. We summarize all aspects of regulatory mechanisms underlying the expression and activity of PD-1 and PD-L1 in cancers, including genetic, epigenetic, post-transcriptional and post-translational regulatory mechanisms. In addition, we further summarize the progress in clinical research on the antitumor effects of targeting PD-1/PD-L1 antibodies alone and in combination with other therapeutic approaches, providing new strategies for finding new tumor markers and developing combined therapeutic approaches.

Indexed as

B7-H1 AntigenNeoplasmsProgrammed Cell Death 1 ReceptorAnimalsGene Expression Regulation, NeoplasticHumansSignal TransductionB7-H1 AntigenCD274 protein, humanPDCD1 protein, humanProgrammed Cell Death 1 ReceptorCombination therapyPD-1PD-L1Regulatory mechanismTumor immunity

Identifiers

PMID38762484
PMCPMC11102195

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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.