Evidence map›Paper›PMID 19508171›Full record

ReviewCurrent cancer drug targets2009

The role of fibroblast growth factors in tumor growth.

M Korc, R E Friesel

Open access · greenAbstract readReview
In one paragraph

Review in Current cancer drug targets, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
161citing papers in PubMed, 1 pooled it
7.9field-weighted citation impact, top 2% 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

161 citing papers in PubMed, 1 synthesis or guideline pooled it, 357 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Human FGF1Cells · 2026
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  10. The FGF/FGFR/c-Myc axis as a promising therapeutic target in multiple myeloma.Journal of experimental & clinical cancer research : CR · 2024
    Review
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101 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

M KorcDepartment of Medicine, Dartmouth Hitchcock Medical Center, Lebanon, NH 03756, USA. Murray.Korc@Dartmouth.edu
R E Friesel
Dartmouth–Hitchcock Medical Center · US

Funding

Transcriptional Decisions in Endothelial Cell DifferentiationP20RR015555 · NCRR · MAINE MEDICAL CENTER · PI PRUDOVSKY, IGOR · 2000 to 2009
$21.4M
Novel aspects of Epithelial-Mesenchymal Transition(EMT)in pancreatic cancerR01CA075059 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI KORC, MURRAY · 1997 to 2018
$4.3M
Feedback Inhibitory Mechanisms in Skeletal DevelopmentR01DK073871 · NIDDK · MAINEHEALTH · PI FRIESEL, ROBERT E · 2007 to 2011
$1.7M
Role of Glypican-1 in Pancreatic CancerR01CA101306 · NCI · UNIVERSITY OF CALIFORNIA IRVINE · PI KORC, MURRAY · 2003 to 2007
$1.7M
NCI NIH HHS CA-101306NCI NIH HHS CA-750509NCI NIH HHS R01 CA075059NCI NIH HHS R01 CA101306NCRR NIH HHS P20 RR015555NCRR NIH HHS RR-15555NIDDK NIH HHS DK-73871NIDDK NIH HHS R01 DK073871
6 · The paper itself

Abstract

Biological processes that drive cell growth are exciting targets for cancer therapy. The fibroblast growth factor (FGF) signaling network plays a ubiquitous role in normal cell growth, survival, differentiation, and angiogenesis, but has also been implicated in tumor development. Elucidation of the roles and relationships within the diverse FGF family and of their links to tumor growth and progression will be critical in designing new drug therapies to target FGF receptor (FGFR) pathways. Recent studies have shown that FGF can act synergistically with vascular endothelial growth factor (VEGF) to amplify tumor angiogenesis, highlighting that targeting of both the FGF and VEGF pathways may be more efficient in suppressing tumor growth and angiogenesis than targeting either factor alone. In addition, through inducing tumor cell survival, FGF has the potential to overcome chemotherapy resistance highlighting that chemotherapy may be more effective when used in combination with FGF inhibitor therapy. Furthermore, FGFRs have variable activity in promoting angiogenesis, with the FGFR-1 subgroup being associated with tumor progression and the FGFR-2 subgroup being associated with either early tumor development or decreased tumor progression. This review highlights the growing knowledge of FGFs in tumor cell growth and survival, including an overview of FGF intracellular signaling pathways, the role of FGFs in angiogenesis, patterns of FGF and FGFR expression in various tumor types, and the role of FGFs in tumor progression.

Indexed as

AnimalsCell SurvivalFibroblast Growth FactorsGenetic Diseases, InbornHumansMiceMice, KnockoutModels, BiologicalNeoplasm MetastasisNeoplasmsNeovascularization, PathologicReceptors, Fibroblast Growth FactorSignal TransductionVascular Endothelial Growth Factor AFibroblast Growth FactorsReceptors, Fibroblast Growth FactorVascular Endothelial Growth Factor A

Identifiers

PMID19508171
PMCPMC3664927
OpenAlexW2035743945

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.