ArticleOncogene2011
IL-3 is a novel target to interfere with tumor vasculature.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Integration of healthy volunteers in early phase clinical trials with immuno-oncological compounds.Frontiers in oncology · 2022Pooled it
- Fueling the Seed: Growth Factors and Cytokines Driving Cancer Stem Cells in Gynecological Malignancies.International journal of molecular sciences · 2025Review
- Monophosphoryl Lipid A-2,4-Dinitrophenylamine Conjugates Are Potent Adjuvants for Carbohydrate and Protein Vaccines.JACS Au · 2025Article
- Interleukins as a potential link between obstructive sleep apnea and renal cell carcinoma.Contemporary oncology (Poznan, Poland) · 2025Review
- Effect of colony‑stimulating factor in the mechanism of bone metastasis development (Review).Oncology reports · 2024Review
- Proliferating macrophages in human tumours show characteristics of monocytes responding to myelopoietic growth factors.Frontiers in immunology · 2024Article
- Long-term Effects of the pituitary-adenylate cyclase-activating Polypeptide (PACAP38) in the Adult Mouse Retina: Microglial Activation and Induction of Neural Proliferation.Neurochemical research · 2023Article
- Review
- Article
- Network controllability solutions for computational drug repurposing using genetic algorithms.Scientific reports · 2022Article
- Review
- Cancer-associated cells release citrate to support tumour metastatic progression.Life science alliance · 2021Article
- Transcriptome of rhesus macaque (Macaca mulatta) exposed to total-body irradiation.Scientific reports · 2021Article
- Tumor Immune Evasion Induced by Dysregulation of Erythroid Progenitor Cells Development.Cancers · 2021Review
- Targeting IL-3Rα on tumor-derived endothelial cells blunts metastatic spread of triple-negative breast cancer via extracellular vesicle reprogramming.Oncogenesis · 2020Article
- Nicotinamide inhibits melanoma in vitro and in vivo.Journal of experimental & clinical cancer research : CR · 2020Article
- Assessment of faithful interleukin-3 production by novel bicistronic interleukin-3 reporter mice.Immunology letters · 2020Article
- The Tumor Milieu Promotes Functional Human Tumor-Resident Plasmacytoid Dendritic Cells in Humanized Mouse Models.Frontiers in immunology · 2020Article
- Anti-CTLA-4 synergizes with dendritic cell-targeted vaccine to promote IL-3-dependent CD4Annals of the New York Academy of Sciences · 2019Article
- The pro- and anti-tumor roles of mesenchymal stem cells toward BRCA1-IRIS-overexpressing TNBC cells.Breast cancer research : BCR · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Angiogenesis inhibiting agents are currently integral component of anticancer therapy. However, tumors, initially responsive to anti-angiogenic drugs or vascular targeting agents, can acquire resistance. The limited clinical efficacy might result from the heterogeneous nature of tumors or alternatively from the unique phenotype of tumor vascular cells, widely diverse from so-called 'normal' endothelium. Hence, defining the molecular mechanisms driving this diversity might provide a rational basis to design combinatory therapies that should be more effective in avoiding resistance. Herein, we demonstrated that tumor-derived endothelial cells (TECs) isolated from breast and kidney carcinomas retained an endothelial phenotype, but outspread independently of growth factors. Applying small interfering RNA approach, we demonstrated that interleukin (IL)-3, but not vascular endothelial growth factor, released by TECs, supports their autocrine growth and promotes in vivo vessel formation and tumor angiogenesis. Meanwhile, we found that the expression of the membrane-bound kit ligand (mbKitL) depends on IL-3, and it is crucial for adhesion of endothelial progenitor cells (EPCs) and inflammatory cells to TECs. These events required Akt activation. Finally, the finding that depletion of the mbKitL prevented EPC and inflammatory cell trafficking into vascular microenvironment, indicates that, as in bone marrow, the mbKitL can act as a membrane/adhesion molecule for c-Kit-expressing cells. These data provide evidences that an IL-3 autocrine loop can drive a tumor endothelial switch and that targeting IL-3 might confer a significant therapeutic advantage to hamper tumor angiogenesis.
Indexed as
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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.