ArticleCancer research2015
CD38-Expressing Myeloid-Derived Suppressor Cells Promote Tumor Growth in a Murine Model of Esophageal Cancer.
Article in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
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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
114 citing papers in PubMed, 163 citations in OpenAlex.
- A phase 1/2, open-label, multicenter study of isatuximab in combination with cemiplimab in patients with lymphoma.Hematological oncology · 2023Trial
- Trial
- Research progress on the compositional characteristics of the tumor immune microenvironment and immunopredictive models in esophageal squamous cell carcinoma.Cancer biology & therapy · 2026Review
- Targeting VEGF signaling and stromal remodeling enhances chemoimmunotherapy efficacy in esophageal cancer.Journal for immunotherapy of cancer · 2026Article
- CD38 overexpression drives glioblastoma progression via L1CAM/ICAM1/JAK-STAT-Driven tumor microenvironment rewiring.Translational oncology · 2026Article
- Bidirectional Interactions Between Immune Regulation and the Insulin-like Growth Factor Axis in Colorectal Cancer.International journal of molecular sciences · 2026Review
- Targeting of CD28 and CD38 as a potential novel therapeutic strategy for peripheral T-cell lymphomas.Scientific reports · 2026Article
- Virus-based IFNγ gene delivery and photodynamic therapy cooperate to remodel the tumor microenvironment and suppress breast cancer.Molecular therapy. Oncology · 2026Article
- Immune-Centered Cross-Talk Between Cancer Cells and the Tumor Microenvironment-Implications for Therapy.Cancers · 2026Review
- CD38+ NK cells: novel players in immunoregulation.Frontiers in immunology · 2026Review
- Immunosuppressive tumor microenvironment and immunotherapy resistance of esophageal carcinoma.Frontiers in immunology · 2026Review
- Overcoming chemoresistance in esophageal cancer with synergistic strategies.Frontiers in immunology · 2026Review
- Regulating the regulators via targeting CD38 in the tumor microenvironment.Frontiers in immunology · 2026Review
- Modulation of Human Immune Cells by Propyl-Propane Thiosulfonate (PTSO) Inhibits Colorectal Tumor Progression in a Humanized Mouse Model.Nutrients · 2025Article
- Unmasking immune checkpoint resistance in esophageal squamous cell carcinoma: Insights into the tumor microenvironment and biomarker landscape.World journal of gastrointestinal oncology · 2025Review
- Epigenomic preconditioning of peripheral monocytes determines their transcriptional response to the tumor microenvironment.Genome medicine · 2025Article
- CD38 contributes to tumor progression and tumor microenvironment reshaping in epithelial ovarian cancer.Translational oncology · 2025Article
- Tumor suppressors in Sox2-mediated lung cancers promote distinct cell-intrinsic and immunologic remodeling.JCI insight · 2025Article
- Exploring the causal relationship between immune factors and chondrosarcoma: a Mendelian randomization study.Discover oncology · 2025Article
- Review
54 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Myeloid-derived suppressor cells (MDSC) are an immunosuppressive population of immature myeloid cells found in advanced-stage cancer patients and mouse tumor models. Production of inducible nitric oxide synthase (iNOS) and arginase, as well as other suppressive mechanisms, allows MDSCs to suppress T-cell-mediated tumor clearance and foster tumor progression. Using an unbiased global gene expression approach in conditional p120-catenin knockout mice (L2-cre;p120ctn(f/f)), a model of oral-esophageal cancer, we have identified CD38 as playing a vital role in MDSC biology, previously unknown. CD38 belongs to the ADP-ribosyl cyclase family and possesses both ectoenzyme and receptor functions. It has been described to function in lymphoid and early myeloid cell differentiation, cell activation, and neutrophil chemotaxis. We find that CD38 expression in MDSCs is evident in other mouse tumor models of esophageal carcinogenesis, and CD38(high) MDSCs are more immature than MDSCs lacking CD38 expression, suggesting a potential role for CD38 in the maturation halt found in MDSC populations. CD38(high) MDSCs also possess a greater capacity to suppress activated T cells, and promote tumor growth to a greater degree than CD38(low) MDSCs, likely as a result of increased iNOS production. In addition, we have identified novel tumor-derived factors, specifically IL6, IGFBP3, and CXCL16, which induce CD38 expression by MDSCs ex vivo. Finally, we have detected an expansion of CD38(+) MDSCs in peripheral blood of advanced-stage cancer patients and validated targeting CD38 in vivo as a novel approach to cancer therapy.
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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.