Evidence map›Paper›PMID 36859386›Full record

ReviewMolecular cancer2023

CD39/CD73/A2AR pathway and cancer immunotherapy.

Chenglai Xia, Shuanghong Yin, Kenneth K W To, Liwu Fu

Open access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 254 papers.

0numbers the graph read from it
0cells of the map it votes in
254citing papers in PubMed
78.8field-weighted citation impact, top 1% of its field
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

254 citing papers in PubMed, 306 citations in OpenAlex.

  1. Trial
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  4. From danger to resolution: targeting purinergic signaling in CNS diseases.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
    Review
  5. Article
  6. Macrophage Trogocytosis of Tumor Cells Drives the Immunosuppression of Tumor Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Engineering the next generation of cellular therapies for solid tumors: multi-specific armored CARs and TME reprogramming strategies.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  13. γδ T cells in colorectal and liver cancer.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  14. Article
  15. Article
  16. Review
  17. Article
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  19. Article
  20. Review

194 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

4 authors at 4 institutions in 1 country.

Chenglai XiaAffiliated Foshan Maternity and Child Healthcare Hospital, Southern Medical University, Foshan, 528000, China. xiachenglai@smu.edu.cn.
Shuanghong YinAffiliated Foshan Maternity and Child Healthcare Hospital, Southern Medical University, Foshan, 528000, China.
Kenneth K W ToSchool of Pharmacy, The Chinese University of Hong Kong, Hong Kong, China.
Liwu FuState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangdong Esophageal Cancer Institute, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China. fulw@mail.sysu.edu.cn.
Chinese University of Hong Kong · CNSouthern Medical University · CNSun Yat-sen University · CNSun Yat-sen University Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer development is closely associated with immunosuppressive tumor microenvironment (TME) that attenuates antitumor immune responses and promotes tumor cell immunologic escape. The sequential conversion of extracellular ATP into adenosine by two important cell-surface ectonucleosidases CD39 and CD73 play critical roles in reshaping an immunosuppressive TME. The accumulated extracellular adenosine mediates its regulatory functions by binding to one of four adenosine receptors (A1R, A2AR, A2BR and A3R). The A2AR elicits its profound immunosuppressive function via regulating cAMP signaling. The increasing evidence suggests that CD39, CD73 and A2AR could be used as novel therapeutic targets for manipulating the antitumor immunity. In recent years, monoclonal antibodies or small molecule inhibitors targeting the CD39/CD73/A2AR pathway have been investigated in clinical trials as single agents or in combination with anti-PD-1/PD-L1 therapies. In this review, we provide an updated summary about the pathophysiological function of the adenosinergic pathway in cancer development, metastasis and drug resistance. The targeting of one or more components of the adenosinergic pathway for cancer therapy and circumvention of immunotherapy resistance are also discussed. Emerging biomarkers that may be used to guide the selection of CD39/CD73/A2AR-targeting treatment strategies for individual cancer patients is also deliberated.

Indexed as

ImmunotherapyNeoplasmsAdenosineAntibodies, MonoclonalCell MembraneHumansAdenosineAntibodies, MonoclonalA2ARAdenosine receptorCancer immunotherapyCD39CD73Immunosuppressive tumor microenvironment

Identifiers

PMID36859386
PMCPMC9979453
OpenAlexW4322758207

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.