ArticleProceedings of the National Academy of Sciences of the United States of America2016
Solid tumor therapy by selectively targeting stromal endothelial cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 44 citations in OpenAlex.
- Lipid metabolic plasticity in glioblastoma: mechanisms, tumor microenvironment remodeling, and therapeutic opportunities.Frontiers in oncology · 2026Review
- Protective antigen-mediated delivery of an anti-CRISPR protein for precision genome editing.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- ERK pathway reactivation prevents anthrax toxin lethality in mice.Nature microbiology · 2025Article
- ATP depletion in anthrax edema toxin pathogenesis.PLoS pathogens · 2025Article
- Angiogenesis, a key point in the association of gut microbiota and its metabolites with disease.European journal of medical research · 2024Review
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- Lipid metabolic rewiring in glioma‑associated microglia/macrophages (Review).International journal of molecular medicine · 2024Review
- ERK and c-Myc signaling in host-derived tumor endothelial cells is essential for solid tumor growth.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Targeting reactive oxygen species and fat acid oxidation for the modulation of tumor-associated macrophages: a narrative review.Frontiers in immunology · 2023Review
- Article
- ANTXR1 as a potential prognostic biomarker for hepatitis B virus-related hepatocellular carcinoma identified by a weighted gene correlation network analysis.Journal of gastrointestinal oncology · 2021Article
- An in vivo selection-derived d-peptide for engineering erythrocyte-binding antigens that promote immune tolerance.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- IgG-Engineered Protective Antigen for Cytosolic Delivery of Proteins into Cancer Cells.ACS central science · 2021Article
- Anthrax lethal factor cleaves regulatory subunits of phosphoinositide-3 kinase to contribute to toxin lethality.Nature microbiology · 2020Article
- Inhibitory Effects of a Reengineered Anthrax Toxin on Canine and Human Osteosarcoma Cells.Toxins · 2020Article
- Targeting Cancer Gene Dependencies with Anthrax-Mediated Delivery of Peptide Nucleic Acids.ACS chemical biology · 2020Article
- Article
- Article
- Gastric Cancer Tumor Microenvironment Characterization Reveals Stromal-Related Gene Signatures Associated With Macrophage Infiltration.Frontiers in genetics · 2020Article
- Bismaleimide cross-linked anthrax toxin forms functional octamers with high specificity in tumor targeting.Protein science : a publication of the Protein Society · 2019Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Engineered tumor-targeted anthrax lethal toxin proteins have been shown to strongly suppress growth of solid tumors in mice. These toxins work through the native toxin receptors tumor endothelium marker-8 and capillary morphogenesis protein-2 (CMG2), which, in other contexts, have been described as markers of tumor endothelium. We found that neither receptor is required for tumor growth. We further demonstrate that tumor cells, which are resistant to the toxin when grown in vitro, become highly sensitive when implanted in mice. Using a range of tissue-specific loss-of-function and gain-of-function genetic models, we determined that this in vivo toxin sensitivity requires CMG2 expression on host-derived tumor endothelial cells. Notably, engineered toxins were shown to suppress the proliferation of isolated tumor endothelial cells. Finally, we demonstrate that administering an immunosuppressive regimen allows animals to receive multiple toxin dosages and thereby produces a strong and durable antitumor effect. The ability to give repeated doses of toxins, coupled with the specific targeting of tumor endothelial cells, suggests that our strategy should be efficacious for a wide range of solid tumors.
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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.