Evidence map›Paper›PMID 37627061›Full record

ArticleCancers2023

Preclinical Evaluation of the FGFR-Family Inhibitor Futibatinib for Pediatric Rhabdomyosarcoma.

Jerry T Wu, Adam Cheuk, Kristine Isanogle, Christina Robinson, Xiaohu Zhang, Michele Ceribelli, Erin Beck, Paul Shinn, Carleen Klumpp-Thomas, Kelli M Wilson and 17 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

10 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Fusion-Negative Rhabdomyosarcoma: Clinical Application of Targeted RNA Sequencing.Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
    Article
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

27 authors at 5 institutions in 2 countries.

Jerry T WuGenetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Adam CheukGenetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Kristine IsanogleLaboratory Animal Sciences Program, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA.
Christina RobinsonLaboratory Animal Sciences Program, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA.
Xiaohu ZhangNational Center for Advancing Translational Sciences, Rockville, MD 20850, USA.
Michele CeribelliNational Center for Advancing Translational Sciences, Rockville, MD 20850, USA.
Erin BeckNational Center for Advancing Translational Sciences, Rockville, MD 20850, USA.
Paul ShinnNational Center for Advancing Translational Sciences, Rockville, MD 20850, USA.
Carleen Klumpp-ThomasNational Center for Advancing Translational Sciences, Rockville, MD 20850, USA.
Kelli M WilsonNational Center for Advancing Translational Sciences, Rockville, MD 20850, USA.ORCID 0000-0003-2636-2766
Crystal McKnightNational Center for Advancing Translational Sciences, Rockville, MD 20850, USA.
Zina ItkinNational Center for Advancing Translational Sciences, Rockville, MD 20850, USA.
Hiroshi SotomeTaiho Pharmaceutical Co., Ltd., Tsukuba 300-0034, Japan.
Hiroshi HiraiTaiho Pharmaceutical Co., Ltd., Tsukuba 300-0034, Japan.
Elizabeth CallejaTaiho Oncology, Princeton, NJ 08540, USA.
Volker WacheckTaiho Oncology, Princeton, NJ 08540, USA.
Brad GoukerLaboratory Animal Sciences Program, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA.
Cody J PeerClinical Pharmacology Program, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0001-9395-3473
Natalia CorvalanClinical Pharmacology Program, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0009-0003-3722-7903
David MilewskiGenetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0002-9778-8548
Yong Y KimGenetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
William D FiggClinical Pharmacology Program, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0003-2428-5613
Elijah F EdmondsonLaboratory Animal Sciences Program, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA.ORCID 0000-0002-6106-3705
Craig J ThomasNational Center for Advancing Translational Sciences, Rockville, MD 20850, USA.
Simone DifilippantonioLaboratory Animal Sciences Program, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA.
Jun S WeiGenetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0002-4812-0250
Javed KhanGenetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0002-5858-0488
National Center for Advancing Translational Sciences · USNational Institutes of Health · USFrederick National Laboratory for Cancer Research · USTaiho Oncology (United States) · USTaiho Pharmaceutical (Japan) · JP

Funding

NCI NIH HHS HHSN261201500003CNCI NIH HHS HHSN261201500003I
6 · The paper itself

Abstract

Rhabdomyosarcoma (RMS) is the most common pediatric soft tissue sarcoma. Despite decades of clinical trials, the overall survival rate for patients with relapsed and metastatic disease remains below 30%, underscoring the need for novel treatments. FGFR4, a receptor tyrosine kinase that is overexpressed in RMS and mutationally activated in 10% of cases, is a promising target for treatment. Here, we show that futibatinib, an irreversible pan-FGFR inhibitor, inhibits the growth of RMS cell lines in vitro by inhibiting phosphorylation of FGFR4 and its downstream targets. Moreover, we provide evidence that the combination of futibatinib with currently used chemotherapies such as irinotecan and vincristine has a synergistic effect against RMS in vitro. However, in RMS xenograft models, futibatinib monotherapy and combination treatment have limited efficacy in delaying tumor growth and prolonging survival. Moreover, limited efficacy is only observed in a PAX3-FOXO1 fusion-negative (FN) RMS cell line with mutationally activated FGFR4, whereas little or no efficacy is observed in PAX3-FOXO1 fusion-positive (FP) RMS cell lines with FGFR4 overexpression. Alternative treatment modalities such as combining futibatinib with other kinase inhibitors or targeting FGFR4 with CAR T cells or antibody-drug conjugate may be more effective than the approaches tested in this study.

Indexed as

FGFR4FGFR inhibitorfutibatinibpediatric cancerrhabdomyosarcoma

Identifiers

PMID37627061
PMCPMC10452847
OpenAlexW4385708196

What OpenQuestion holds

Textmetadata
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.