ArticlePloS one2019
Monitoring and characterizing soluble and membrane-bound ectonucleotidases CD73 and CD39.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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.
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.
Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- PUF family RNA-binding proteins Puf1 and Puf2 promote transcript degradation in Toxoplasma gondii.The Journal of biological chemistry · 2026Article
- Adenosine Signaling as a Central Integrative Network in Cellular Stress Responses and a Therapeutically Actionable Target in Human Disease.Biomolecules · 2026Review
- CD39 and CD73: biological functions, diseases and therapy.Molecular biomedicine · 2025Review
- Identification of 6‑Aryl-7-Deazapurine Ribonucleoside Phosphonates as Inhibitors of Ecto-5'-Nucleotidase (CD73).ACS pharmacology & translational science · 2025Article
- Developing a risk score using liquid biopsy biomarkers for selecting Immunotherapy responders and stratifying disease progression risk in metastatic melanoma patients.Journal of experimental & clinical cancer research : CR · 2025Article
- Immunometabolic editing of the tumor microenvironment: from reprogramming mechanisms to therapeutic vulnerabilities.Frontiers in immunology · 2025Review
- Purinergic regulation of pulmonary vascular tone.Purinergic signalling · 2024Review
- CD39 Is Expressed on Functional Effector and Tissue-resident Memory CD8+ T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Mathematical modeling of hypoxia and adenosine to explore tumor escape mechanisms in DC-based immunotherapy.Scientific reports · 2024Article
- Circulating Ectonucleotidases Signal Impaired Myocardial Perfusion at Rest and Stress.Journal of the American Heart Association · 2023Article
- CD39/CD73/A2AR pathway and cancer immunotherapy.Molecular cancer · 2023Review
- Review
- Mono(ADP-ribosyl)ation Enzymes and NADCells · 2021Review
- A Novel CD73 Inhibitor SHR170008 Suppresses Adenosine in Tumor and Enhances Anti-Tumor Activity with PD-1 Blockade in a Mouse Model of Breast Cancer.OncoTargets and therapy · 2021Article
- Selective monitoring of the protein-free ADP-ribose released by ADP-ribosylation reversal enzymes.PloS one · 2021Article
- Co-localization and confinement of ecto-nucleotidases modulate extracellular adenosine nucleotide distributions.PLoS computational biology · 2020Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The success of immunotherapy treatment in oncology ushered a new modality for treating a wide variety of cancers. However, lack of effect in some patients made it imperative to identify other pathways that are exploited by cancer cells to circumvent immune surveillance, and possibly synergize immune checkpoint treatment in those cases. It has been recently recognized that adenosine levels increase significantly in the tumor microenvironment and that adenosine/adenosine receptors play a powerful role as immunosuppressive and attenuating several effector T cell functions. The two main enzymes responsible for generating adenosine in the microenvironment are the ectonucleotidases CD39 and CD73, the former utilizes both ATP and ADP and produces AMP while the latter utilizes AMP and generates adenosine. Thus, these two enzymes combined are the major source for the bulk of adenosine produced in the microenvironment. They were shown to be validated targets in oncology leading to several clinical trials that include small molecules as well as antibodies, showing positive and encouraging results in the preclinical arena. Towards the development of novel drugs to target these enzymes, we have developed a platform that can be utilized to monitor the activities of both enzymes in vitro (biochemical) as well as in cells (cell based) assays. We have developed very sensitive and homogenous assays that enabled us to monitor the activity of both enzymes and demonstrate selectivity of known inhibitors as well as monoclonal antibodies. This should speed up screening for novel inhibitors that might lead to more effective cancer therapy.
Indexed as
Identifiers
What OpenQuestion holds
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.