ArticleOncotarget2015
A non-canonical adenosinergic pathway led by CD38 in human melanoma cells induces suppression of T cell proliferation.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
What it found
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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
70 citing papers in PubMed, 93 citations in OpenAlex.
- Phase II clinical and immune correlate study of adjuvant nivolumab plus ipilimumab for high-risk resected melanoma.Journal for immunotherapy of cancer · 2022Trial
- Nucleotide Metabolism in Health and Disease.MedComm · 2026Review
- Emerging chemical strategies for CD38 inhibition: restoring NADBioorganic & medicinal chemistry · 2026Review
- Rapid Discovery of CD38 Inhibitor via DNA-Encoded Natural Product Library Screening.Molecules (Basel, Switzerland) · 2026Article
- The CD73-adenosine axis in melanoma: from multidimensional regulation to precision immunotherapy.Frontiers in immunology · 2026Review
- Modulating CD38 enzymatic activity during antibody-based immunotherapy in multiple myeloma: a basic science perspective.Frontiers in immunology · 2026Article
- Regulating the regulators via targeting CD38 in the tumor microenvironment.Frontiers in immunology · 2026Review
- Article
- Overcoming resistance to immunotherapy by targeting CD38 in human tumor explants.Cell reports. Medicine · 2025Article
- Single-cell and spatial genomic landscape of non-small cell lung cancer brain metastases.Nature medicine · 2025Article
- Review
- Illuminating the impact of CD38-induced adenosine formation in B-cell lymphoma.Scientific reports · 2025Article
- Changes in CD4Clinical and experimental medicine · 2025Article
- Cutaneous melanoma and purinergic modulation by phenolic compounds.Purinergic signalling · 2024Review
- CD38 as theranostic target in oncology.Journal of translational medicine · 2024Review
- Resistance mechanisms and potential therapeutic strategies in relapsed or refractory natural killer/T cell lymphoma.Chinese medical journal · 2024Review
- Disrupting CD38-driven T cell dysfunction restores sensitivity to cancer immunotherapy.bioRxiv : the preprint server for biology · 2024Article
- Unraveling the Intricacies of CD73/Adenosine Signaling: The Pulmonary Immune and Stromal Microenvironment in Lung Cancer.Cancers · 2023Review
- B-cell targeting with anti-CD38 daratumumab: implications for differentiation and memory responses.Life science alliance · 2023Article
- The interplay between the DNA damage response and ectonucleotidases modulates tumor response to therapy.Science immunology · 2023Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nucleotide-metabolizing ectoenzymes are endowed with an extracellular catalytic domain, which is involved in regulating the extracellular nucleotide/nucleoside balance. The tumor microenvironment contains high levels of adenosine (ADO) generated by this enzymatic network, thus promoting tumor growth by inhibiting anti-tumor immune responses. ADO inhibition in melanoma murine models limits tumor metastases and restores anti-tumor immune responses. This work investigates the expression and function of ectoenzymes in primary human melanoma cell lines. All of latter cells expressed CD38, CD39, CD73, and CD203a/PC-1, and produced ADO from AMP and NAD(+ )T cell proliferation. Accordingly, phosphorylation of S6 ribosomal protein, p38 and Stat1 was lower in activated memory cells than in naïve CD4(+) T lymphocytes. Melanoma cells also inhibited proliferation of naïve, memory and -to a lesser extent- of effector CD8(+) T cells. These different inhibitory effects correlated with distinct patterns of expression of the ADO receptor A2a and A2b. These results show that primary human melanoma cell lines suppress in vitro T cell proliferation through an adenosinergic pathway in which CD38 and CD73 play a prominent role.
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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.