Evidence map›Paper›PMID 28258700›Full record

ReviewImmunological reviews2017

The ectonucleotidases CD39 and CD73: Novel checkpoint inhibitor targets.

Bertrand Allard, Maria Serena Longhi, Simon C Robson, John Stagg

Abstract readReview
In one paragraph

Review in Immunological reviews, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 606 papers.

0numbers the graph read from it
0cells of the map it votes in
606citing papers in PubMed
55.5field-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

606 citing papers in PubMed, 863 citations in OpenAlex.

  1. Trial
  2. Trial
  3. CD39 on CD8European journal of immunology · 2026
    Review
  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
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  14. AC3Medical oncology (Northwood, London, England) · 2026
    Article
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546 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 2 countries.

Bertrand AllardCentre de Recherche du Centre Hospitalier de l'Université de Montréal et Institut du Cancer de Montréal, Montréal, QC, Canada.
Maria Serena LonghiDivisions of Gastroenterology and Transplantation, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Simon C RobsonDivisions of Gastroenterology and Transplantation, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
John StaggCentre de Recherche du Centre Hospitalier de l'Université de Montréal et Institut du Cancer de Montréal, Montréal, QC, Canada.
Beth Israel Deaconess Medical Center · USCentre Hospitalier de l’Université de Montréal · CAHarvard University · USUniversité de Montréal · CA

Funding

Therapeutic assessment of synthetic heparin sulfates in transplantation modelsP01HL107152 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI DESAI, UMESH RAMANLAL · 2011 to 2017
$15.8M
Role of enteric glia in the death of neurons during gut inflammationR01DK103723 · NIDDK · MICHIGAN STATE UNIVERSITY · PI BRIAN D. GULBRANSEN · 2015 to 2026
$4.7M
Thromboregulatory strategies to prolong xenograft survival.U01AI066331 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ROBSON, SIMON C. · 2005 to 2009
$4.1M
Purinergic ThromboregulationR01HL094400 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ROBSON, SIMON C. · 2009 to 2010
$1.4M
Directed Purinergic Signaling as Immunotherapy in LeukemiaR21CA221702 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI AVIGAN, DAVID E., ROBSON, SIMON C. · 2018 to 2019
$413k
Engineering Inhibitory Antibodies to Ectoenzymes for Cancer TreatmentR21CA164970 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ROBSON, SIMON C. · 2012 to 2013
$405k
CIHRNCI NIH HHS R21 CA164970NCI NIH HHS R21 CA221702NHLBI NIH HHS P01 HL107152NHLBI NIH HHS R01 HL094400NIAID NIH HHS U01 AI066331NIDDK NIH HHS R01 DK103723
6 · The paper itself

Abstract

Cancers are able to grow by subverting immune suppressive pathways, to prevent the malignant cells as being recognized as dangerous or foreign. This mechanism prevents the cancer from being eliminated by the immune system and allows disease to progress from a very early stage to a lethal state. Immunotherapies are newly developing interventions that modify the patient's immune system to fight cancer, by either directly stimulating rejection-type processes or blocking suppressive pathways. Extracellular adenosine generated by the ectonucleotidases CD39 and CD73 is a newly recognized "immune checkpoint mediator" that interferes with anti-tumor immune responses. In this review, we focus on CD39 and CD73 ectoenzymes and encompass aspects of the biochemistry of these molecules as well as detailing the distribution and function on immune cells. Effects of CD39 and CD73 inhibition in preclinical and clinical studies are discussed. Finally, we provide insights into potential clinical application of adenosinergic and other purinergic-targeting therapies and forecast how these might develop in combination with other anti-cancer modalities.

Indexed as

5'-NucleotidaseAnimalsAntibodies, MonoclonalAntigens, CDApyraseClinical Trials as TopicCombined Modality TherapyDrug Evaluation, PreclinicalGPI-Linked ProteinsHumansImmunotherapyNeoplasmsTumor EscapeTumor Microenvironment5'-NucleotidaseAntibodies, MonoclonalAntigens, CDApyraseCD39 antigenGPI-Linked ProteinsNT5E protein, humancancer inflammationimmunityimmunotherapies monocytes/macrophagesT cellstumor

Identifiers

PMID28258700
PMCPMC5338647
OpenAlexW2591655768

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.