Evidence map›Paper›PMID 39979991›Full record

ArticleBMC urology2025

GATA3 amplification is associated with high grade disease in non-invasive urothelial bladder cancer but unrelated to patient prognosis.

Henning Plage, Adrian Frericks, Sebastian Hofbauer, Kira Furlano, Sarah Weinberger, Florian Roßner, Simon Schallenberg, Sefer Elezkurtaj, Maximilian Lennartz, Andreas Marx and 16 more

Abstract read
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In one paragraph

Article in BMC urology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. 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

26 authors.

Henning PlageDepartment of Urology, Charité- Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany. henning.plage@charite.de.ORCID https://orcid.org/0000-0002-7680-1870
Adrian FrericksInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Sebastian HofbauerDepartment of Urology, Charité- Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.
Kira FurlanoDepartment of Urology, Charité- Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.
Sarah WeinbergerDepartment of Urology, Charité- Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.
Florian RoßnerInstitute of Pathology, Charité- Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Berlin, Germany.
Simon SchallenbergInstitute of Pathology, Charité- Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Berlin, Germany.
Sefer ElezkurtajInstitute of Pathology, Charité- Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Berlin, Germany.
Maximilian LennartzInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Andreas MarxDepartment of Pathology, Academic Hospital Fuerth, Fuerth, Germany.
Henrik SamtlebenDepartment of Pathology, Academic Hospital Fuerth, Fuerth, Germany.
Margit FischDepartment of Urology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Michael RinkDepartment of Urology, Marien Hospital Hamburg, Hamburg, Germany.
Marcin SlojewskiDepartment of Urology and Urological Oncology, Pomeranian Medical University, Szczecin, Poland.
Krystian KaczmarekDepartment of Urology and Urological Oncology, Pomeranian Medical University, Szczecin, Poland.
Thorsten EckeDepartment of Urology, Helios Hospital Bad Saarow, Bad Saarow, Germany.
Stefan KochDepartment of Pathology, Helios Hospital Bad Saarow, Bad Saarow, Germany.
Ronald SimonInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Guido SauterInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Henrik ZechaDepartment of Urology, Albertinen Hospital, Hamburg, Germany.
Joachim WeischenfeldtDepartment of Urology, Charité- Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.
Tobias KlatteDepartment of Urology, Helios Hospital Bad Saarow, Bad Saarow, Germany.
Sarah MinnerInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
David HorstInstitute of Pathology, Charité- Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Berlin, Germany.
Thorsten SchlommDepartment of Urology, Charité- Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.
Martina KluthInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeWe aimed to assess the impact of GATA3 binding protein (GATA3) gene copy number alterations on tumor aggressiveness, patient prognosis, and GATA3 protein expression in a large urothelial bladder cancer cohort.

methodsA tissue microarray containing over 2,700 urothelial bladder cancers (pTa-pT4) was analyzed retrospectively using dual-labeling fluorescence in-situ hybridization (FISH) with probes for GATA3 (10p14) and centromere 10. GATA3 copy number gains were categorized as GATA3 elevation (ratio GATA3/centromere ≥ 2/≤4), low-level amplification (ratio > 4/≤12), and high-level amplification (ratio > 12) and deletions were divided between homozygous and heterozygous.

resultsGATA3 copy number gain was detected in 9.9% of 2,213 interpretable tumors, including 2.0% with GATA3 elevation, 3.2% with low-level amplification, and 4.7% with high-level amplification. The frequency of high-level amplification increased from pTa G2 low (0%) to pTa G3 tumors (12% [CI 0.07;0.21]; p < 0.0001 pTa G2 low vs. pTaG2 high) but decreased in advanced-stage carcinomas pT2-4 with 5.4% [CI 0.07;0.21] (p < 0.0001, pTa vs. pT2-4). In muscle-invasive carcinomas, GATA3 amplification was not linked to tumor aggressiveness or patient survival. Overall, no homozygous GATA3 deletion was detected and heterozygous GATA3 deletion was only observed in 1.1%; of 1,432 pT2-4 tumors without any association to cancer progression. While GATA3 copy number was significantly correlated with GATA3 expression (p < 0.0001), the relationship was not strong. Only 2.3% of GATA3-negative cancers had a deletion, and 42.1% of strong GATA3-expressing cancers exhibited high-level amplification.

conclusionHigh-level GATA3 amplification is common in urothelial bladder cancer and correlates with grade progression in pTa tumors, while GATA3 deletion is rare. Neither amplification nor deletion appears to be the primary driver of GATA3 expression dysregulation. CLINICAL TRIAL NUMBER: Not applicable.

Indexed as

Carcinoma, Transitional CellGATA3 Transcription FactorGene AmplificationUrinary Bladder NeoplasmsAgedAged, 80 and overCohort StudiesFemaleHumansMaleMiddle AgedNeoplasm GradingPrognosisRetrospective StudiesGATA3 protein, humanGATA3 Transcription FactorFISHGATA3PrognosisUrothelial bladder cancer

Identifiers

PMID39979991
PMCPMC11841250

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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.