ReviewBiochemical pharmacology2021
Targeting ectonucleotidases to treat inflammation and halt cancer development in the gut.
Review in Biochemical pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed, 13 citations in OpenAlex.
- PI3Kdelta-driven expansion of regulatory B cells impairs protective immune responses to Trypanosoma congolense parasite infection.PLoS pathogens · 2025Article
- Cd39 and P2rx7-Wnt signaling enhance blast pathogenicity in an experimental model of acute myeloid leukemia.Haematologica · 2025Article
- T Cell-Derived Apoptotic Extracellular Vesicles Ameliorate Bone Loss via CD39 and CD73-Mediated ATP Hydrolysis.International journal of nanomedicine · 2025Article
- Targeting chemoresistance and mitochondria-dependent metabolic reprogramming in acute myeloid leukemia.Frontiers in oncology · 2023Review
- Transcriptome profiling of PBMCs and formalin-fixed autopsy tissues from COVID-19 patients.STAR protocols · 2022Article
- Purinergic and Adenosinergic Signaling in Pancreatobiliary Diseases.Frontiers in physiology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
CD39 and CD73 control cell immunity by hydrolyzing proinflammatory ATP and ADP (CD39) into AMP, subsequently converted into anti-inflammatory adenosine (CD73). By regulating the balance between effector and regulatory cells, these ectonucleotidases promote immune homeostasis in acute and chronic inflammation; while also appearing to limit antitumor effector immunity in gut cancer. This manuscript focuses on the pivotal role of CD39 and CD73 ectonucleotidase function in shaping immune responses in the gut. We focus on those mechanisms deployed by these critical and pivotal ectoenzymes and the regulation in the setting of gastrointestinal tract infections, inflammatory bowel disease and tumors of the gastrointestinal tract. We will highlight translational and clinical implications of the latest and most innovative basic research discoveries of these important players of the purinergic signaling. Immunotherapeutic strategies that have been developed to either boost or control ectonucleotidase expression and activity in important disease settings are also reviewed and the in vivo effects discussed.
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.