Evidence map›Paper›PMID 26224133›Full record

ReviewCancer metastasis reviews2015

Fibroblast growth factor receptor signaling in hereditary and neoplastic disease: biologic and clinical implications.

Teresa Helsten, Maria Schwaederle, Razelle Kurzrock

Open access · hybridAbstract readReview
In one paragraph

Review in Cancer metastasis reviews, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

84 citing papers in PubMed, 129 citations in OpenAlex.

  1. Trial
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  4. Towards biomarker-driven therapies for urothelial carcinoma.Nature reviews. Clinical oncology · 2026
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  5. Advancements in targeted therapy for gastric cancer.Therapeutic advances in gastroenterology · 2026
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  11. Tumour-agnostic kinase inhibitors.Nature reviews. Drug discovery · 2025
    Review
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  18. Article
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24 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

3 authors at 1 institution in 1 country.

Teresa HelstenCenter for Personalized Cancer Therapy and Division of Hematology and Oncology, University of California San Diego, Moores Cancer Center, 3855 Health Sciences Drive, MC #0658, La Jolla, CA, 92093-0658, USA. thelsten@ucsd.edu.
Maria SchwaederleCenter for Personalized Cancer Therapy and Division of Hematology and Oncology, University of California San Diego, Moores Cancer Center, 3855 Health Sciences Drive, MC #0658, La Jolla, CA, 92093-0658, USA. mschwaederle@ucsd.edu.
Razelle KurzrockCenter for Personalized Cancer Therapy and Division of Hematology and Oncology, University of California San Diego, Moores Cancer Center, 3855 Health Sciences Drive, MC #0658, La Jolla, CA, 92093-0658, USA.
University of California, San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibroblast growth factors (FGFs) and their receptors (FGFRs) are transmembrane growth factor receptors with wide tissue distribution. FGF/FGFR signaling is involved in neoplastic behavior and also development, differentiation, growth, and survival. FGFR germline mutations (activating) can cause skeletal disorders, primarily dwarfism (generally mutations in FGFR3), and craniofacial malformation syndromes (usually mutations in FGFR1 and FGFR2); intriguingly, some of these activating FGFR mutations are also seen in human cancers. FGF/FGFR aberrations reported in cancers are mainly thought to be gain-of-function changes, and several cancers have high frequencies of FGFR alterations, including breast, bladder, or squamous cell carcinomas (lung and head and neck). FGF ligand aberrations (predominantly gene amplifications) are also frequently seen in cancers, in contrast to hereditary syndromes. There are several pharmacologic agents that have been or are being developed for inhibition of FGFR/FGF signaling. These include both highly selective inhibitors as well as multi-kinase inhibitors. Of note, only four agents (ponatinib, pazopanib, regorafenib, and recently lenvatinib) are FDA-approved for use in cancer, although the approval was not based on their activity against FGFR. Perturbations in the FGFR/FGF signaling are present in both inherited and malignant diseases. The development of potent inhibitors targeting FGF/FGFR may provide new tools against disorders caused by FGF/FGFR alterations.

Indexed as

Fibroblast Growth FactorsGenetic Diseases, InbornHumansMutationNeoplasmsReceptors, Fibroblast Growth FactorSignal TransductionFibroblast Growth FactorsReceptors, Fibroblast Growth FactorCancerCancer therapyFGFFGFRGenetics

Identifiers

PMID26224133
PMCPMC4573649
OpenAlexW1861063348

What OpenQuestion holds

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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.