Evidence map›Paper›PMID 17297442›Full record

ArticleOncogene2007

Conditional activation of FGFR1 in the prostate epithelium induces angiogenesis with concomitant differential regulation of Ang-1 and Ang-2.

S F Winter, V D Acevedo, R D Gangula, K W Freeman, D M Spencer, N M Greenberg

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Targeting fibroblast growth factor pathways in prostate cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013
    Review
  11. The FGF/FGFR axis as a therapeutic target in breast cancer.Expert review of endocrinology & metabolism · 2013
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  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

6 authors at 3 institutions in 2 countries.

S F WinterClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.
V D Acevedo
R D Gangula
K W Freeman
D M Spencer
N M Greenberg
Baylor College of Medicine · USFred Hutch Cancer Center · USHarvard University · US

Funding

Initiative for Maximizing Student Development (IMSD) ProgramR25GM056929 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI PEREIRA, FRED A · 1998 to 2023
$12.4M
KGF IN PROSTATE CANCER--A TRANSGENIC ANIMAL MODELR01CA064851 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GREENBERG, NORMAN MICHAEL · 1994 to 2008
$2.7M
NCI NIH HHS CA64851NIGMS NIH HHS R25 GM056929
6 · The paper itself

Abstract

The expression of fibroblast growth factor receptor (FGFR)-1 correlates with angiogenesis and is associated with prostate cancer (CaP) progression. To more precisely define the molecular mechanisms whereby FGFR1 causes angiogenesis in the prostate we exploited a transgenic mouse model, JOCK-1, in which activation of a conditional FGFR1 allele in the prostate epithelium caused rapid angiogenesis and progressive hyperplasia. By labeling the vasculature in vivo and applying a novel method to measure the vasculature in three dimensions, we were able to observe a significant increase in vascular volume 1 week after FGFR1 activation. Although vessel volume and branching both continued to increase throughout a 6-week period of FGFR1 activation, importantly, we discovered that continued activation of FGFR1 was not required to maintain the new vasculature. Exploring the molecular mediators of the angiogenic phenotype, we observed consistent upregulation of HIF-1alpha, vascular endothelial growth factor (VEGF) and angiopoietin 2 (Ang-2), whereas expression of Ang-1 was lost. Further analysis revealed that loss of Ang-1 expression occurred in the basal epithelium, whereas the increase in Ang-2 expression occurred in the luminal epithelium. Reporter assays confirmed that the Ang-2 promoter was regulated by FGFR1 signaling and a small molecule inhibitor of FGFR activity, PD173074, could abrogate this response. These findings establish a method to follow spontaneous angiogenesis in a conditional autochthonous system, implicate the angiopoietins as downstream effectors of FGFR1 activation in vivo, and suggest that therapies targeting FGFR1 could be used to inhibit neovascularization during initiation and progression of CaP.

Indexed as

Neovascularization, PhysiologicAngiopoietin-1Angiopoietin-2AnimalsCell LineEpitheliumMaleMiceMice, TransgenicProstateReceptor, Fibroblast Growth Factor, Type 1Signal TransductionTranscriptional ActivationAngiopoietin-1Angiopoietin-2Angpt1 protein, mouseReceptor, Fibroblast Growth Factor, Type 1

Identifiers

PMID17297442
OpenAlexW1990110300

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.