Evidence map›Paper›PMID 38424198›Full record

ReviewNature reviews. Clinical oncology2024

FGFR-targeted therapeutics: clinical activity, mechanisms of resistance and new directions.

Masuko Katoh, Yohann Loriot, Giovanni Brandi, Simona Tavolari, Zev A Wainberg, Masaru Katoh

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Clinical oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed
35.5field-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.

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

101 citing papers in PubMed, 152 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Blockade of FGFR1 Trafficking to the Cell Surface Results in the Partial Mistargeting of the Receptor to Peroxisomes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Cytokines and cancer-associated fibroblasts.Journal of hematology & oncology · 2026
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

41 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

6 authors at 4 institutions in 4 countries.

Masuko KatohM & M Precision Medicine, Tokyo, Japan.
Yohann LoriotDrug Development Department (DITEP), Institut Gustave Roussy, Université Paris-Saclay, Villejuif, France.ORCID http://orcid.org/0000-0001-7162-6869
Giovanni BrandiMedical Oncology, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy.ORCID http://orcid.org/0000-0003-0013-2858
Simona TavolariMedical Oncology, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy.
Zev A WainbergDepartment of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Masaru KatohM & M Precision Medicine, Tokyo, Japan. mkatoh-kkr@umin.ac.jp.ORCID http://orcid.org/0000-0003-3274-4066
Azienda USL di Bologna · ITNational Cancer Centre Japan · JPInserm · FRUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibroblast growth factor (FGF) signalling via FGF receptors (FGFR1-4) orchestrates fetal development and contributes to tissue and whole-body homeostasis, but can also promote tumorigenesis. Various agents, including pan-FGFR inhibitors (erdafitinib and futibatinib), FGFR1/2/3 inhibitors (infigratinib and pemigatinib), as well as a range of more-specific agents, have been developed and several have entered clinical use. Erdafitinib is approved for patients with urothelial carcinoma harbouring FGFR2/3 alterations, and futibatinib and pemigatinib are approved for patients with cholangiocarcinoma harbouring FGFR2 fusions and/or rearrangements. Clinical benefit from these agents is in part limited by hyperphosphataemia owing to off-target inhibition of FGFR1 as well as the emergence of resistance mutations in FGFR genes, activation of bypass signalling pathways, concurrent TP53 alterations and possibly epithelial-mesenchymal transition-related isoform switching. The next generation of small-molecule inhibitors, such as lirafugratinib and LOXO-435, and the FGFR2-specific antibody bemarituzumab are expected to have a reduced risk of hyperphosphataemia and the ability to overcome certain resistance mutations. In this Review, we describe the development and current clinical role of FGFR inhibitors and provide perspective on future research directions including expansion of the therapeutic indications for use of FGFR inhibitors, combination of these agents with immune-checkpoint inhibitors and the application of novel technologies, such as artificial intelligence.

Indexed as

Bile Duct NeoplasmsCarcinoma, Transitional CellCholangiocarcinomaHyperphosphatemiaUrinary Bladder NeoplasmsArtificial IntelligenceBile Ducts, IntrahepaticHumansProtein Kinase InhibitorsProtein Kinase Inhibitors

Identifiers

PMID38424198
OpenAlexW4392284056

What OpenQuestion holds

Textmetadata
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.