Evidence map›Paper›PMID 39167629›Full record

ReviewJournal of advanced research2024

Deciphering the role of CD47 in cancer immunotherapy.

Yu'e Liu, Linjun Weng, Yanjin Wang, Jin Zhang, Qi Wu, Pengcheng Zhao, Yufeng Shi, Ping Wang, Lan Fang

Abstract readReview
In one paragraph

Review in Journal of advanced research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
–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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed.

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  8. Molecular Insights and Novel Therapies for Lymphoproliferative Disorders.International journal of molecular sciences · 2026
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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

9 authors.

Yu'e LiuTongji University Cancer Center, Shanghai Tenth People's Hospital of Tongji University, School of Medicine, Tongji University, Shanghai 200092, China.
Linjun WengTongji University Cancer Center, Shanghai Tenth People's Hospital of Tongji University, School of Medicine, Tongji University, Shanghai 200092, China.
Yanjin WangDepartment of Nephrology, Shanghai East Hospital, Tongji University, School of Medicine, Shanghai, China.
Jin ZhangDepartment of Pharmacology and Toxicology, University of Mississippi, Medical Center, 39216 Jackson, MS, USA.
Qi WuTongji University Cancer Center, Shanghai Tenth People's Hospital of Tongji University, School of Medicine, Tongji University, Shanghai 200092, China.
Pengcheng ZhaoSchool of Life Sciences and Medicine, Shandong University of Technology, No.266 Xincun West Road, Zibo 255000, Shandong Province, China.
Yufeng ShiTongji University Cancer Center, Shanghai Tenth People's Hospital of Tongji University, School of Medicine, Tongji University, Shanghai 200092, China; Clinical Center for Brain and Spinal Cord Research, Tongji University, Shanghai 200092, China. Electronic address: yshi@tongji.edu.cn.
Ping WangTongji University Cancer Center, Shanghai Tenth People's Hospital of Tongji University, School of Medicine, Tongji University, Shanghai 200092, China. Electronic address: wangp@tongji.edu.cn.
Lan FangTongji University Cancer Center, Shanghai Tenth People's Hospital of Tongji University, School of Medicine, Tongji University, Shanghai 200092, China. Electronic address: lanfang@tongji.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundImmunotherapy has emerged as a novel strategy for cancer treatment following surgery, radiotherapy, and chemotherapy. Immune checkpoint blockade and Chimeric antigen receptor (CAR)-T cell therapies have been successful in clinical trials. Cancer cells evade immune surveillance by hijacking inhibitory pathways via overexpression of checkpoint genes. The Cluster of Differentiation 47 (CD47) has emerged as a crucial checkpoint for cancer immunotherapy by working as a "don't eat me" signal and suppressing innate immune signaling. Furthermore, CD47 is highly expressed in many cancer types to protect cancer cells from phagocytosis via binding to SIRPα on phagocytes. Targeting CD47 by either interrupting the CD47-SIRPα axis or combing with other therapies has been demonstrated as an encouraging therapeutic strategy in cancer immunotherapy. Antibodies and small molecules that target CD47 have been explored in pre- and clinical trials. However, formidable challenges such as the anemia and palate aggregation cannot be avoided because of the wide presentation of CD47 on erythrocytes. AIM OF VIEW: This review summarizes the current knowledge on the regulation and function of CD47, and provides a new perspective for immunotherapy targeting CD47. It also highlights the clinical progress of targeting CD47 and discusses challenges and potential strategies. KEY SCIENTIFIC CONCEPTS OF REVIEW: This review provides a comprehensive understanding of targeting CD47 in cancer immunotherapy, it also augments the concept of combination immunotherapy strategies by employing both innate and adaptive immune responses.

Indexed as

CD47 AntigenImmunotherapyNeoplasmsAnimalsAntigens, DifferentiationHumansImmunity, InnatePhagocytosisReceptors, ImmunologicSignal TransductionAntigens, DifferentiationCD47 AntigenCD47 protein, humanReceptors, ImmunologicSIRPA protein, humanCD47CD47-SIRPαImmunotherapyPhagocytosis

Identifiers

PMID39167629
PMCPMC11380025

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.