Evidence map›Paper›PMID 24327018›Full record

ArticleBritish journal of cancer2014

Enhanced FGFR signalling predisposes pancreatic cancer to the effect of a potent FGFR inhibitor in preclinical models.

H Zhang, B L Hylander, C LeVea, E A Repasky, R M Straubinger, A A Adjei, W W Ma

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 57 citations in OpenAlex.

  1. FGFR Inhibitor AZD4547 Disrupts Inflammatory CAF Crosstalk With Cancer Cells and Macrophages and Attenuates Metastasis in Pancreatic Cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  5. Fibroblast growth factor receptor 1 inhibition suppresses pancreatic cancer chemoresistance and chemotherapy-driven aggressiveness.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2024
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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.

H ZhangDepartment of Medicine, Roswell Park Cancer Institute, Elm & Carlton streets, Buffalo, NY 14263, USA.
B L HylanderDepartment of Immunity, Roswell Park Cancer Institute, Elm & Carlton streets, Buffalo, NY 14263, USA.
C LeVeaDepartment of Medicine, Roswell Park Cancer Institute, Elm & Carlton streets, Buffalo, NY 14263, USA.
E A RepaskyDepartment of Immunity, Roswell Park Cancer Institute, Elm & Carlton streets, Buffalo, NY 14263, USA.
R M StraubingerDepartment of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, State University of New York at Buffalo, Buffalo, NY, USA.
A A AdjeiDepartment of Medicine, Roswell Park Cancer Institute, Elm & Carlton streets, Buffalo, NY 14263, USA.
W W MaDepartment of Medicine, Roswell Park Cancer Institute, Elm & Carlton streets, Buffalo, NY 14263, USA.
University at Buffalo, State University of New York · US

Funding

Two-Spirit Films in Indigenous Cancer HealthP30CA016056 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI MARK G FRATTINI · 1985 to 2026
$116.6M
NCI NIH HHS P30 CA016056
6 · The paper itself

Abstract

backgroundFibroblast growth factor receptor (FGFR) signalling has been implicated in pancreas carcinogenesis. We investigated the effect of FGFR inhibition in pancreatic cancer in complementary cancer models derived from cell lines and patient-derived primary tumour explants.

methodsThe effects of FGFR signalling inhibition in pancreatic cancer were evaluated using anti-FRS2 shRNA and dovitinib. Pancreatic cancers with varying sensitivity to dovitinib were evaluated to determine potential predictive biomarkers of efficacy. Primary pancreatic explants with opposite extreme of biomarker expression were selected from 13 tumours for in vivo dovitinib treatment.

resultsTreatment with anti-FRS2 shRNA induced significant in vitro cell kill in pancreatic cancer cells. Dovitinib treatment achieved similar effects and was mediated by Akt/Mcl-1 signalling in sensitive cells. Dovitinib efficacy correlated with FRS2 phosphorylation status, FGFR2 mRNA level and FGFR2 IIIb expression but not phosphorylation status of VEGFR2 and PDGFRβ. Using FGFR2 mRNA level, a proof-of-concept study using primary pancreatic cancer explants correctly identified the tumours' sensitivity to dovitinib.

conclusionInhibiting FGFR signalling using shRNA and dovitinib achieved significant anti-cancer cancer effects in pancreatic cancer. The effect was more pronounced in FGFR2 IIIb overexpressing pancreatic cancer that may be dependent on aberrant stimulation by stromal-derived FGF ligands.

Indexed as

Adaptor Proteins, Signal TransducingApoptosisBenzimidazolesBiomarkers, TumorCarcinogenesisCell Line, TumorDrug Evaluation, PreclinicalHumansMembrane ProteinsMyeloid Cell Leukemia Sequence 1 ProteinPancreatic NeoplasmsPhosphorylationProto-Oncogene Proteins c-aktQuinolonesReceptor, Fibroblast Growth Factor, Type 2Receptor, Platelet-Derived Growth Factor beta4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-oneAdaptor Proteins, Signal TransducingBenzimidazolesBiomarkers, TumorFGFR2 protein, humanFRS2 protein, humanMCL1 protein, humanMembrane ProteinsMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene Proteins c-aktQuinolonesReceptor, Fibroblast Growth Factor, Type 2Receptor, Platelet-Derived Growth Factor betaRNA, Small Interfering

Identifiers

PMID24327018
PMCPMC3899776
OpenAlexW2014266189

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.