Evidence map›Paper›PMID 20066901›Full record

ArticleOncology research2009

VEGF165 promotes the osteolytic bone destruction of ewing's sarcoma tumors by upregulating RANKL.

Hui Guan, Zhichao Zhou, Ying Cao, Xiaoping Duan, Eugenie S Kleinerman

Open access · hybridAbstract read
In one paragraph

Article in Oncology research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Targeting VEGF and Its Receptors for the Treatment of Osteoarthritis and Associated Pain.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2016
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Bisphosphonate therapy in pediatric patients.Journal of diabetes and metabolic disorders · 2014
    Review
  13. Article
  14. Article
  15. 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

5 authors at 1 institution in 1 country.

Hui GuanDivision of Pediatrics, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.
Zhichao Zhou
Ying Cao
Xiaoping Duan
Eugenie S Kleinerman
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Vasculogenesis in Ewing's Sarcoma: useintherapyR01CA103986 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KLEINERMAN, EUGENIE S · 2004 to 2012
$1.9M
NCI NIH HHS CA16672NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA103986
6 · The paper itself

Abstract

The purpose of this study was to determine whether vascular endothelial growth factor-165 (VEGF165) contributed to the osteolytic process in Ewing's sarcoma. VEGF165 induced osteoclast formation from murine bone marrow cells. Tartrate-resistant acid phosphatase (TRAP) staining demonstrated significantly fewer osteoclasts in VEGF-inhibited TC/siVEGF7-1 tumors compared to TC71 parental or TC/si-control tumors. Receptor activator NF-kappaB (RANKL), a critical osteoclastogenic factor, was decreased in TC/siVEGF7-1 cells. Incubation of these cells with recombinant VEGF165 upregulated RANKL in a dose- and time-dependent manner. The induction of (RANKL) by VEGF165 was also demonstrated in MC3T3-E1 mouse osteoblast cells and bone marrow stromal cells. This upregulation was transcriptionally mediated by an effect on the RANKL promoter. Both VEGF and EWS/FLI-1 increased RANKL promoter activity. Taken together, these data suggest that modulation of RANKL by VEGF165 may be one of the mechanisms responsible for the osteolytic process induced by Ewing's sarcoma cells. VEGF165 may, therefore, play an important role in modulating RANKL gene expression in the bone marrow microenvironment during the metastatic process, thereby contribution to tumor induced bone lysis.

Indexed as

OsteolysisAnimalsCell Line, TumorGene Expression Regulation, NeoplasticHumansMiceMice, Inbred BALB CMicrofilament ProteinsOsteoclastsPromoter Regions, GeneticRANK LigandReceptors, Cytoplasmic and NuclearRNA-Binding Protein EWSSarcoma, EwingTrans-ActivatorsUp-RegulationFLII protein, humanMicrofilament ProteinsRANK LigandReceptors, Cytoplasmic and NuclearRNA-Binding Protein EWSTrans-ActivatorsVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID20066901
PMCPMC2875875
OpenAlexW2012622419

What OpenQuestion holds

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Registered trials

None linked

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.