ArticleImmunotherapy2014
Requirement of NK cells for selective A2A receptor blockade to suppress CD73+ tumor metastasis.
Article in Immunotherapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 14 citations in OpenAlex.
- Inhibitors of the CD73-adenosinergic checkpoint as promising combinatory agents for conventional and advanced cancer immunotherapy.Frontiers in immunology · 2023Review
- A prognostic signature based on adenosine metabolism related genes for ovarian cancer.Frontiers in oncology · 2022Article
- Varied functions of immune checkpoints during cancer metastasis.Cancer immunology, immunotherapy : CII · 2021Review
- Article
- Targeting CD73 to augment cancer immunotherapy.Current opinion in pharmacology · 2020Review
- A2A adenosine receptor antagonists to weaken the hypoxia-HIF-1α driven immunosuppression and improve immunotherapies of cancer.Current opinion in pharmacology · 2016Review
- Anti-CD73 in cancer immunotherapy: awakening new opportunities.Trends in cancer · 2016Article
- A2aR antagonists: Next generation checkpoint blockade for cancer immunotherapy.Computational and structural biotechnology journal · 2015Review
Corrections and comments
- Comment on
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Evaluation of: Beavis PA, Divisekera U, Paget C et al. Blockade of A2A receptors potently suppresses the metastasis of CD73(+) tumors. Proc. Natl Acad. Sci. USA 110(36), 14711-14716 (2013). CD73 is becoming an emerging therapeutic target for the prevention of tumor growth and metastasis. However, the mechanism by which CD73 promotes tumor metastasis is unclear. Beavis et al. evaluated the efficacy of A2A and A2B adenosine receptor antagonists in inhibiting the metastasis of tumors expressing CD73, either endogenously or ectopically. They demonstrate distinct mechanisms whereby A2A versus A2B adenosine receptors could contribute to CD73(+) tumor metastasis. As A2Areceptor (R)/A2BR antagonists have been tested in clinical trials in other disease settings, this study highlights the potential therapeutic application of an A2AR/A2BR blockade strategy for treatment of CD73(+) metastatic tumors.
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.