ArticleNeoplasia (New York, N.Y.)2011
NK1.1 cells and CD8 T cells mediate the antitumor activity of Cl-IB-MECA in a mouse melanoma model.
Article in Neoplasia (New York, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Molecular basis of ligand binding and receptor activation at the human ANature communications · 2025Article
- Tumor site-directed A1R expression enhances CAR T cell function and improves efficacy against solid tumors.Nature communications · 2025Article
- 2‑Cl‑IB‑MECA regulates the proliferative and drug resistance pathways, and facilitates chemosensitivity in pancreatic and liver cancer cell lines.International journal of molecular medicine · 2022Article
- A Novel Antagonistic CD73 Antibody for Inhibition of the Immunosuppressive Adenosine Pathway.Molecular cancer therapeutics · 2021Article
- AFrontiers in oncology · 2021Article
- Review
- Inhibition of the adenosinergic pathway: the indispensable part of oncological therapy in the future.Purinergic signalling · 2019Review
- Targeting Adenosine Receptor Signaling in Cancer Immunotherapy.International journal of molecular sciences · 2018Review
- Purinergic Signalling: Therapeutic Developments.Frontiers in pharmacology · 2017Review
- AC-1001 H3 CDR peptide induces apoptosis and signs of autophagy in vitro and exhibits antimetastatic activity in a syngeneic melanoma model.FEBS open bio · 2016Article
- Myeloid-derived suppressor cells contribute to A2B adenosine receptor-induced VEGF production and angiogenesis in a mouse melanoma model.Oncotarget · 2015Article
- Growth and metastasis of B16-F10 melanoma cells is not critically dependent on host CD73 expression in mice.BMC cancer · 2014Article
- Adenosine limits the therapeutic effectiveness of anti-CTLA4 mAb in a mouse melanoma model.American journal of cancer research · 2014Article
- Cancer subclonal genetic architecture as a key to personalized medicine.Neoplasia (New York, N.Y.) · 2013Article
- Blockade of A2b adenosine receptor reduces tumor growth and immune suppression mediated by myeloid-derived suppressor cells in a mouse model of melanoma.Neoplasia (New York, N.Y.) · 2013Article
- Purinergic signalling and cancer.Purinergic signalling · 2013Review
- Blockade of A2A receptors potently suppresses the metastasis of CD73+ tumors.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- The adenosinergic system in cancer: Key therapeutic target.Oncoimmunology · 2013Article
- Overcoming intratumor heterogeneity of polygenic cancer drug resistance with improved biomarker integration.Neoplasia (New York, N.Y.) · 2012Article
- Adoptive immunotherapy with Cl-IB-MECA-treated CD8+ T cells reduces melanoma growth in mice.PloS one · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Cl-IB-MECA, synthetic A(3) adenosine receptor agonist, is a potential anticancer agent. In this study, we have examined the effect of Cl-IB-MECA in a mouse melanoma model. Cl-IB-MECA significantly inhibited tumor growth in immune-competent mice. Notably, the number of tumor-infiltrating NK1.1(+) cells and CD8(+) T cells was significantly increased in Cl-IB-MECA-treated mice. This effect was correlated with high levels of tumor necrosis factor α (TNF-α) and interferon γ in melanoma tissue. Depletion of either CD8(+) T cells or NK1.1(+) cells completely abrogated the antitumor effect of Cl-IB-MECA. Accordingly, Cl-IB-MECA did not affect tumor growth in nude mice. In addition, we also found that the number of mature and active conventional dendritic cells at the tumor site was increased after Cl-IB-MECA administration. Moreover, Cl-IB-MECA significantly increased TNF-α and IL-12p40 release from splenic CD11c(+) cells. In conclusion, our study provides novel insights into the mechanism by which Cl-IB-MECA leads to an effective antitumor response that involves the activation of natural killer cells and CD8(+) T cells and further highlights its therapeutic potential.
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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.