Evidence map›Paper›PMID 24265351›Full record

ReviewAnnals of oncology : official journal of the European Society for Medical Oncology2014

Genomic aberrations in the FGFR pathway: opportunities for targeted therapies in solid tumors.

R Dienstmann, J Rodon, A Prat, J Perez-Garcia, B Adamo, E Felip, J Cortes, A J Iafrate, P Nuciforo, J Tabernero

Registry-linked trialAbstract readReview
In one paragraph

Review in Annals of oncology : official journal of the European Society for Medical Oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05019794 (A Phase IIa of Infigratinib in Subjects With Locally Advanced or Metastatic Gastric Cancer or Gastroesophageal Junction Adenocarcinoma With FGFR2 Amplification or Other Advanced Solid Tumors With Other FGFR Alterations), which is not on this map. Cited by 209 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
209citing papers in PubMed, 3 pooled it
13.0field-weighted citation impact, top 1% 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.

NCT05019794 phase2unknown statusnot on this mapstarted 2020, after this paper: background citation

A Phase IIa of Infigratinib in Subjects With Locally Advanced or Metastatic Gastric Cancer or Gastroesophageal Junction Adenocarcinoma With FGFR2 Amplification or Other Advanced Solid Tumors With Other FGFR Alterations

TypeinterventionalSponsorLianBio LLCRan2020 to 2023Enrolled80ConditionsGastric Cancer, Gastroesophageal Junction Adenocarcinoma, Solid TumorArmsInfigratinib
3 · Its place in the literature

Who cites it

209 citing papers in PubMed, 3 syntheses or guidelines pooled it, 361 citations in OpenAlex.

  1. Pooled it
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  15. PI3Kα Inhibitor and Degrader Inavolisib Can Co-opt FGFR2 to Enhance Responses in Patients with PIK3CA-Mutated Solid Tumors and in Preclinical Models.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
  16. Article
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  19. World journal of gastrointestinal oncology · 2025
    Article
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149 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

10 authors at 3 institutions in 1 country.

R DienstmannMolecular Pathology Lab, Massachusetts General Hospital Cancer Center, Boston, USA.
J RodonMedical Oncology Department.
A PratMedical Oncology Department; Translational Genomics Lab.
J Perez-GarciaMedical Oncology Department.
B AdamoMedical Oncology Department.
E FelipMedical Oncology Department.
J CortesMedical Oncology Department.
A J IafrateMolecular Pathology Lab, Massachusetts General Hospital Cancer Center, Boston, USA.
P NuciforoMolecular Oncology Lab, Vall d'Hebron Institute of Oncology, Barcelona, Spain.
J TaberneroMedical Oncology Department. Electronic address: jtabernero@vhebron.net.
Massachusetts General Hospital · USTranslational Genomics Research Institute · USVall d'Hebron Institute of Oncology

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The fibroblast growth factor receptor (FGFR) cascade plays crucial roles in tumor cell proliferation, angiogenesis, migration and survival. Accumulating evidence suggests that in some tumor types, FGFRs are bona fide oncogenes to which cancer cells are addicted. Because FGFR inhibition can reduce proliferation and induce cell death in a variety of in vitro and in vivo tumor models harboring FGFR aberrations, a growing number of research groups have selected FGFRs as targets for anticancer drug development. Multikinase FGFR/vascular endothelial growth factor receptor (VEGFR) inhibitors have shown promising activity in breast cancer patients with FGFR1 and/or FGF3 amplification. Early clinical trials with selective FGFR inhibitors, which may overcome the toxicity constraints raised by multitarget kinase inhibition, are recruiting patients with known FGFR(1-4) status based on genomic screens. Preliminary signs of antitumor activity have been demonstrated in some tumor types, including squamous cell lung carcinomas. Rational combination of targeted therapies is expected to further increase the efficacy of selective FGFR inhibitors. Herein, we discuss unsolved questions in the clinical development of these agents and suggest guidelines for management of hyperphosphatemia, a class-specific mechanism-based toxicity. In addition, we propose standardized definitions for FGFR1 and FGFR2 gene amplification based on in situ hybridization methods. Extended access to next-generation sequencing platforms will facilitate the identification of diseases in which somatic FGFR(1-4) mutations, amplifications and fusions are potentially driving cancer cell viability, further strengthening the role of FGFR signaling in cancer biology and providing more possibilities for the therapeutic application of FGFR inhibitors.

Indexed as

Molecular Targeted TherapyAntibodies, MonoclonalFibroblast Growth Factor 3Gene AmplificationHumansHyperphosphatemiaNeoplasmsReceptor, Fibroblast Growth Factor, Type 1Receptor, Fibroblast Growth Factor, Type 2Receptor, Fibroblast Growth Factor, Type 3Receptor, Fibroblast Growth Factor, Type 4Receptors, Vascular Endothelial Growth FactorAntibodies, MonoclonalFGF3 protein, humanFGFR1 protein, humanFGFR2 protein, humanFGFR3 protein, humanFGFR4 protein, humanFibroblast Growth Factor 3Receptor, Fibroblast Growth Factor, Type 1Receptor, Fibroblast Growth Factor, Type 2Receptor, Fibroblast Growth Factor, Type 3Receptor, Fibroblast Growth Factor, Type 4Receptors, Vascular Endothelial Growth Factoramplificationcancerfibroblast growth factor receptor FGFRhyperphosphatemiaoncogenetargeted therapy

Identifiers

PMID24265351
PMCPMC4433501
OpenAlexW2139046059

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.