Evidence map›Paper›PMID 32098829›Full record

ReviewJournal for immunotherapy of cancer2020

On the mechanism of anti-CD39 immune checkpoint therapy.

David Allard, Bertrand Allard, John Stagg

Erratum issuedOpen access · goldAbstract readReview
In one paragraph

Review in Journal for immunotherapy of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
13.0field-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

80 citing papers in PubMed, 135 citations in OpenAlex.

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20 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

David AllardFaculty of Pharmacy, Centre Hospitalier de L'Universite de Montreal, Montreal, Quebec, Canada.
Bertrand AllardInstitut du Cancer de Montreal, Centre Hospitalier de L'Universite de Montreal, Montreal, Quebec, Canada.
John StaggFaculty of Pharmacy, Centre Hospitalier de L'Universite de Montreal, Montreal, Quebec, Canada john.stagg@umontreal.ca.
Centre Hospitalier de l’Université de Montréal · CA

Funding

CIHR
6 · The paper itself

Abstract

With the coming of age of cancer immunotherapy, the search for new therapeutic targets has led to the identification of immunosuppressive adenosine as an important regulator of antitumor immunity. This resulted in the development of selective inhibitors targeting various components of the adenosinergic pathway, including small molecules antagonists targeting the high affinity A2A adenosine receptor and low affinity A2B receptor, therapeutic monoclonal antibodies (mAbs) and small molecules targeting CD73 and therapeutic mAbs targeting CD39. As each regulator of the adenosinergic pathway present non-overlapping biologic functions, a better understanding of the mechanisms of action of each targeted approach should accelerate clinical translation and improve rational design of combination treatments. In this review, we discuss the potential mechanisms-of-action of anti-CD39 cancer therapy and potential toxicities that may emerge from sustained CD39 inhibition. Caution should be taken, however, in extrapolating data from gene-targeted mice to patients treated with blocking anti-CD39 agents. As phase I clinical trials are now underway, further insights into the mechanism of action and potential adverse events associated with anti-CD39 therapy are anticipated in coming years.

Indexed as

AnimalsApyraseHumansImmune Checkpoint InhibitorsImmunotherapyMiceApyraseENTPD1 protein, humanImmune Checkpoint InhibitorsA2AadenosineCD39CD73checkpoint blockadeimmune checkpointimmunotherapy

Identifiers

PMID32098829
PMCPMC7057429
OpenAlexW3006887831

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.