Evidence map›Paper›PMID 39738108›Full record

ArticleNature communications2024

AI allows pre-screening of FGFR3 mutational status using routine histology slides of muscle-invasive bladder cancer.

Pierre-Antoine Bannier, Charlie Saillard, Philipp Mann, Maxime Touzot, Charles Maussion, Christian Matek, Niklas Klümper, Johannes Breyer, Ralph Wirtz, Danijel Sikic and 5 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

16 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  5. Towards biomarker-driven therapies for urothelial carcinoma.Nature reviews. Clinical oncology · 2026
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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

15 authors.

Pierre-Antoine BannierOwkin, Paris, France. pierre-antoine.bannier@owkin.com.ORCID 0009-0008-1175-2976
Charlie SaillardOwkin, Paris, France.ORCID 0000-0003-3061-839X
Philipp MannOwkin, Paris, France.ORCID 0000-0002-2857-4861
Maxime TouzotOwkin, Paris, France.
Charles MaussionOwkin, Paris, France.
Christian MatekInstitute of Pathology, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
Niklas KlümperDepartment of Urology and Pediatric Urology, University Hospital Bonn, Bonn, Germany.
Johannes BreyerDepartment of Urology, St. Caritas Hospital Regensburg, University of Regensburg, Regensburg, Germany.
Ralph WirtzSTRATIFYER Molecular Pathology, Cologne, Germany.
Danijel SikicComprehensive Cancer Center Erlangen-EMN (CCC ER-EMN) and Comprehensive Cancer Center Alliance WERA (CCC WERA), Erlangen, Germany.
Bernd Schmitz-DrägerUrologie 24, St. Theresienkrankenhaus, Nürnberg, Germany.
Bernd WullichComprehensive Cancer Center Erlangen-EMN (CCC ER-EMN) and Comprehensive Cancer Center Alliance WERA (CCC WERA), Erlangen, Germany.
Arndt HartmannInstitute of Pathology, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
Sebastian FörschInstitute of Pathology, University Medical Center Mainz, Johannes Gutenberg-Universität Mainz, Mainz, Germany.ORCID 0000-0002-4740-6900
Markus EcksteinInstitute of Pathology, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. markus.eckstein@uk-erlangen.de.ORCID 0000-0001-5418-3349

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathogenic activating mutations in the fibroblast growth factor receptor 3 (FGFR3) drive disease maintenance and progression in urothelial cancer. 10-15% of muscle-invasive and metastatic urothelial cancer (MIBC/mUC) are FGFR3-mutant. Selective targeting of FGFR3 hotspot mutations with tyrosine kinase inhibitors (e.g., erdafitinib) is approved for mUC and requires FGFR3 mutational testing. However, current testing assays (polymerase chain reaction or next-generation sequencing) necessitate high tissue quality, have long turnover time, and are expensive. To overcome these limitations, we develop a deep-learning model that detects FGFR3 mutations using routine hematoxylin-eosin slides. Encompassing 1222 cases, our study is a large-scale validation of a model prescreening FGFR3 mutations for MIBC and mUC patients. In this work, we demonstrate that our model achieves high sensitivity (>93%) on advanced and metastatic cases while reducing molecular testing by 40% on average, thereby offering a cost-effective and rapid pre-screening tool for identifying patients eligible for FGFR3 targeted therapies.

Indexed as

MutationReceptor, Fibroblast Growth Factor, Type 3Urinary Bladder NeoplasmsAgedDeep LearningDNA Mutational AnalysisFemaleHumansMaleMiddle AgedNeoplasm InvasivenessFGFR3 protein, humanReceptor, Fibroblast Growth Factor, Type 3

Identifiers

PMID39738108
PMCPMC11685973

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.