Evidence map›Paper›PMID 36462464›Full record

ArticleESMO open2022

Pan-tumor landscape of fibroblast growth factor receptor 1-4 genomic alterations.

K Murugesan, A Necchi, T C Burn, O Gjoerup, R Greenstein, M Krook, J A López, M Montesion, H Nimeiri, A R Parikh and 4 more

Open access · goldAbstract read
In one paragraph

Article in ESMO open, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
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  7. Towards biomarker-driven therapies for urothelial carcinoma.Nature reviews. Clinical oncology · 2026
    Review
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  14. Single-center analysis of a real-world cohort of patients with metastatic urothelial carcinoma evaluated by NGS: molecular landscape and efficacy of targeted therapies.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
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  16. Understanding and Overcoming Resistance to Selective FGFR Inhibitors across FGFR2-Driven Malignancies.Clinical cancer research : an official journal of the American Association for Cancer Research · 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

14 authors at 9 institutions in 4 countries.

K MurugesanCancer Genomics Research, Foundation Medicine, Inc., Cambridge, USA.
A NecchiGenitourinary Medical Oncology, Vita-Salute San Raffaele University, Milan; Genitourinary Medical Oncology, IRCCS San Raffaele Hospital and Scientific Institute, Milan, Italy.
T C BurnTranslational and Data Sciences, Incyte Corporation, Wilmington.
O GjoerupScientific and Medical Publications, Foundation Medicine, Inc., Cambridge, USA.
R GreensteinCancer Genomics Research, Foundation Medicine, Inc., Cambridge, USA.
M KrookResearch Scientist, Ohio State University, Columbus, USA.
J A LópezIntegrated Healthcare Solutions, F. Hoffmann-La Roche Ltd, Basel, Switzerland.
M MontesionCancer Genomics Research, Foundation Medicine, Inc., Cambridge, USA.
H NimeiriGlobal Clinical Development Lead Oncology, Foundation Medicine, Inc., Cambridge, USA.
A R ParikhOncology (Medical/Hematology), Jefferson Health, Philadelphia, USA.
S RoychowdhuryMedical Oncology, Ohio State University, Columbus, USA.
S SchwemmersIntegrated HealthCare Solutions PDMA (Oncology), F. Hoffmann-La Roche Ltd, Basel, Switzerland.
I M SilvermanClinical Bioinformatics, Incyte Corporation, Wilmington.
A VogelClinic for Gastroenterology, Hepatology & Endocrinology, Hannover Medical School, Hannover, Germany. Electronic address: Vogel.Arndt@mh-hannover.de.
Cancer Research Foundation · USIncyte (United States) · USRoche (Switzerland) · CHThe Ohio State University · USCambridge Scientific (United States) · USCenter for Global Development · USJefferson Hospital · USMedizinische Hochschule Hannover · DEVita-Salute San Raffaele University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSelective tyrosine kinase inhibitors targeting fibroblast growth factor receptor (FGFR) 1-4 genomic alterations are in development or have been approved for FGFR-altered cancers (e.g. bladder cancer and advanced intrahepatic cholangiocarcinoma). Understanding FGFR inhibitor-resistance mechanisms is increasingly relevant; we surveyed the pan-tumor landscape of FGFR1-4 genomic alterations [short variants (SVs), gene rearrangements (REs), and copy number alterations (CNAs)], including their association with tumor mutational burden (TMB) and the genomic comutational landscape. PATIENTS AND

methodsComprehensive genomic profiling of 355 813 solid tumor clinical cases was performed using the FoundationOne and FoundationOne CDx assays (Foundation Medicine, Inc.) to identify genomic alterations in >300 cancer-associated genes and TMB (determined on ≤1.1 megabases of sequenced DNA).

resultsFGFR1-4 SVs and REs occurred in 9603/355 813 (2.7%), and CNAs in 15 078/355 813 (4.2%) samples. Most common FGFR alterations for bladder cancer, intrahepatic cholangiocarcinoma, and glioma were FGFR3 SVs (1051/7739, 13.6%), FGFR2 REs (618/6641, 9.3%), and FGFR1 SVs (239/11 550, 2.1%), respectively. We found several, potentially clinically relevant, tumor-specific associations between FGFR1-4 genomic alterations and other genomic markers. FGFR3 SV-altered bladder cancers and FGFR1 SV-altered gliomas were significantly less likely to be TMB-high versus unaltered samples. FGFR3 SVs in bladder cancer significantly co-occurred with TERT and CDKN2A/B alterations; TP53 and RB1 alterations were mutually exclusive. In intrahepatic cholangiocarcinoma, FGFR2 REs significantly co-occurred with BAP1 alterations, whereas KRAS, TP53, IDH1, and ARID1A alterations were mutually exclusive. FGFR1 SVs in gliomas significantly co-occurred with H3-3A and PTPN11 alterations, but were mutually exclusive with TERT, EGFR, TP53, and CDKN2A/B alterations.

conclusionsOverall, our hypothesis-generating findings may help to stratify patients in clinical trials and guide optimal targeted therapy in those with FGFR alterations.

Indexed as

Bile Duct NeoplasmsCholangiocarcinomaGliomaUrinary Bladder NeoplasmsBile Ducts, IntrahepaticBiomarkers, TumorGenomicsHumansReceptor, Fibroblast Growth Factor, Type 1Receptor Protein-Tyrosine KinasesBiomarkers, TumorReceptor, Fibroblast Growth Factor, Type 1Receptor Protein-Tyrosine KinasesFGFR1-4FGFR inhibitorsgene rearrangements/fusionsshort variantstargeted therapy

Identifiers

PMID36462464
PMCPMC9832751
OpenAlexW4311033849

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.