Evidence map›Paper›PMID 15655558›Full record

ArticleBritish journal of cancer2005

Evaluation of the fibroblast growth factor system as a potential target for therapy in human prostate cancer.

B Gowardhan, D A Douglas, M E Mathers, A B McKie, S R C McCracken, C N Robson, H Y Leung

Open access · hybridAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of cancer, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.

  1. Pooled it
  2. Potential roles of FGF5 as a candidate therapeutic target in prostate cancer.American journal of clinical and experimental urology · 2023
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Fibroblast growth factors, old kids on the new block.Seminars in cell & developmental biology · 2016
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  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

7 authors at 1 institution in 1 country.

B GowardhanUrology Research Group, Northern Institute for Cancer Research, University of Newcastle, Newcastle upon Tyne, NE2 4HH, UK.
D A Douglas
M E Mathers
A B McKie
S R C McCracken
C N Robson
H Y Leung
Newcastle University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overexpression of fibroblast growth factors (FGFs) has been implicated in prostate carcinogenesis. FGFs function via their high-affinity interactions with receptor tyrosine kinases, FGFR1-4. Expression of FGFR1 and FGFR2 in prostate cancer (CaP) was not found to be associated with clinical parameters. In this report, we further investigated for abnormal FGFR expression in prostate cancer and explore their significance as a potential target for therapy. The expression levels of FGFR3 and FGFR4 in CaP were examined and corroborated to clinical parameters. FGFR3 immunoreactivity in benign prostatic hyperplasia (BPH) and CaP (n=26 and 57, respectively) had similar intensity and pattern. Overall, FGFR4 expression was significantly upregulated in CaP when compared to BPH. A significant positive correlation between FGFR4 expression and Gleason score was noted: Gleason score 7-10 tumours compared to BPH (P<0.0001, Fisher's exact test), Gleason score 4-6 tumours compared to BPH (P<0.0004), and Gleason 7-10 compared to Gleason 4-6 tumours (P<0.005). FGFR4 overexpression was associated with an unfavourable outcome with decreased disease-specific survival (P<0.04, log rank test). FGF-induced signalling is targeted using soluble FGF receptor (sFGFR), potent inhibitor of FGFR function. We have previously shown that sFGFR expression via a replication-deficient adenoviral vector (AdlllcRl) suppresses in vitro FGF-induced signalling and function in human CaP DU145 cells. We tested the significance of inhibiting FGF function along with conventional therapeutic modalities in CaP, and confirmed synergistic effects on in vitro cell growth (proliferation and colony formation) by combining sFGFR expression and treatment with either Paclitaxel (Taxol) or gamma-irradiation. In summary, our data support the model of FGF system as valid target for therapy in CaP.

Indexed as

AgedAged, 80 and overAntineoplastic Agents, PhytogenicDisease-Free SurvivalDrug SynergismDrug Therapy, CombinationFibroblast Growth FactorsHumansImmunohistochemistryMaleMiddle AgedPaclitaxelProstatic HyperplasiaProstatic NeoplasmsRecombinant Fusion ProteinsTumor Cells, CulturedAntineoplastic Agents, PhytogenicFibroblast Growth FactorsPaclitaxelRecombinant Fusion Proteins

Identifiers

PMID15655558
PMCPMC2361833
OpenAlexW2048154391

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.