Evidence map›Paper›PMID 25465225›Full record

ArticleBMC cancer2014

Growth and metastasis of B16-F10 melanoma cells is not critically dependent on host CD73 expression in mice.

Sandra Burghoff, Xuan Gong, Claudia Viethen, Christoph Jacoby, Ulrich Flögel, Sabine Bongardt, Anne Schorr, Andreas Hippe, Bernhard Homey, Jürgen Schrader

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.7field-weighted citation impact, top 12% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 40 citations in OpenAlex.

  1. Tumor-derived RAC1Science advances · 2025
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  4. CD73 contributes to the pathogenesis of fusion-negative rhabdomyosarcoma through the purinergic signaling pathway.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Article
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  7. Article
  8. Article
  9. Article
  10. Review
  11. Varied functions of immune checkpoints during cancer metastasis.Cancer immunology, immunotherapy : CII · 2021
    Review
  12. Characterization of the NPurinergic signalling · 2020
    Article
  13. Article
  14. CD73 (Cluster of Differentiation 73) and the Differences Between Mice and Humans.Arteriosclerosis, thrombosis, and vascular biology · 2019
    Review
  15. Article
  16. Review
  17. Article
  18. The role of extracellular-5'-nucleotidase/CD73 in glioma peritumoural brain edema.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2016
    Article
  19. Purinergic regulation of the immune system.Nature reviews. Immunology · 2016
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Sandra Burghoff
Xuan Gong
Claudia Viethen
Christoph Jacoby
Ulrich Flögel
Sabine Bongardt
Anne Schorr
Andreas Hippe
Bernhard Homey
Jürgen SchraderInstitute of Molecular Cardiology, Heinrich Heine University Duesseldorf, 40225 Duesseldorf, Germany. schrader@uni-duesseldorf.de.
Heinrich Heine University Düsseldorf · DEDüsseldorf University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent studies have suggested that adenosine generated by ecto-5'-nucleotidase (CD73) in the tumor microenvironment plays a major role in promoting tumor growth by suppressing the immune response and stimulating angiogenesis via A2A and A2B receptors. However, adenosine has also been reported to inhibit tumor growth acting via A1 and A3 receptors. Therefore the aim of this study was to clarify the role of host CD73, which catalyzes the extracellular hydrolysis of AMP to adenosine, on tumor growth and metastasis of B16-F10 melanoma cells.

methodsCD73 and alkaline phosphatase (AP) activity of B16-F10 melanoma cells were measured by HPLC. Tumor cells were injected either subcutaneously or intradermally in WT and CD73-/- mice and tumor growth was monitored by MRI at 9.4 T. Immune cell subpopulations within tumors were assessed by FACS after enzymatic digestion. An endothelium specific CD73-/- was created using Tie2-Cre+ mice and CD73flox/flox (loxP) mice. Chimeric mice lacking CD73-/- on hematopoietic cells was generated by bone marrow transplantation. Lung metastatic spread was measured after intravenous B16-F10 application.

resultsB16-F10 cells showed very little CD73 and negligible AP activity. Neither complete loss of host CD73 nor specific knockout of CD73 on endothelial cells or hematopoietic cells affected tumor growth after subcutaneous or intradermal tumor cell application. Only peritumoral edema formation was significantly attenuated in global CD73-/- mice in the intradermal model. Immune cell composition revealed no differences in the different transgenic mice models. Also lung metastasis after intravenous B16-F10 injection was not altered in CD73-/- mice.

conclusionsCD73 expression on host cells, particularly on endothelial and hematopoietic cells, does not modulate tumor growth and metastatic spread of B16-F10 melanoma cells most likely because of insufficient adenosine formation by the tumor itself.

Indexed as

5'-NucleotidaseAnimalsCell Line, TumorFemaleMaleMelanoma, ExperimentalMiceMice, Knockout5'-Nucleotidase

Identifiers

PMID25465225
PMCPMC4265456
OpenAlexW2006227489

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Registered trials

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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.