Evidence map›Paper›PMID 40262102›Full record

ArticlePancreas2025

GATA6 Amplification Is Associated With Improved Survival in TP53-Mutated Unresectable Pancreatic Cancer.

Edward Zhou, Jung-In Yang, Amber N Habowski, Astrid Deschênes, Pascal Belleau, Taehoon Ha, Chris J Tzanavaris, Jeff Boyd, Christopher A Hollweg, Xinhua Zhu and 2 more

Abstract read
In one paragraph

Article in Pancreas, 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. Review
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

12 authors.

Edward ZhouNorthwell Health Cancer Institute, New York, NY.ORCID 0009-0006-7645-2363
Jung-In Yang
Amber N HabowskiCancer Center, Cold Spring Harbor Laboratory, New York, NY.
Astrid DeschênesCancer Center, Cold Spring Harbor Laboratory, New York, NY.
Pascal BelleauCancer Center, Cold Spring Harbor Laboratory, New York, NY.
Taehoon HaCancer Center, Cold Spring Harbor Laboratory, New York, NY.
Chris J TzanavarisDivision of Pulmonary, Critical Care, and Sleep Medicine, Northwell Health, New York, NY.
Jeff BoydNorthwell Health Cancer Institute, New York, NY.
Christopher A HollwegDonald and Barbara Zucker School of Medicine at Hofstra/Northwell, Manhasset, New York, NY.
Xinhua ZhuNorthwell Health Cancer Institute, New York, NY.
David A TuvesonCancer Center, Cold Spring Harbor Laboratory, New York, NY.
Daniel A KingNorthwell Health Cancer Institute, New York, NY.ORCID 0000-0001-6451-712

Funding

Single-Cell Biology Shared ResourceP30CA045508 · NCI · COLD SPRING HARBOR LABORATORY · PI John Edward Moses · 1987 to 2026
$118.9M
NCI NIH HHS P30 CA045508
6 · The paper itself

Abstract

objectivesGATA6 expression is recognized as a favorable prognostic marker of pancreatic cancer, whereas TP53 is a poor prognostic marker. We evaluated treatment outcomes by genetic alterations in TP53 and GATA6 to determine the prognostic and predictive impact of co-alterations. MATERIALS AND

methodsA single institution retrospective analysis was performed on patients diagnosed with pancreatic ductal adenocarcinoma between 2014 and 2023. TP53 genotype and GATA6 amplification status were included in an analysis of overall survival (OS) and progression-free survival (PFS). Previously published patient-derived organoids were used to investigate correlation between genetic status and drug sensitivity.

resultsPatients with TP53 mutations had worse OS compared with the wild-type TP53 population. Patients with GATA6 amplification had better OS and a trend toward better PFS than the nonamplified population. Among patients with a TP53 mutation, patients with GATA6 co-alteration had longer OS compared with those who were not GATA6 amplified. In contrast, among patients who were TP53 wild-type, the presence or absence of a GATA6 amplification did not impact OS or PFS. GATA6 genotype was not associated chemotherapy drug response in an organoid pharmacotyping model.

conclusionsWe found that GATA6 amplification appeared to attenuate poor prognosis observed in TP53-mutant patients regardless of the type of standard chemotherapy received, suggesting the GATA6 amplification is a prognostic biomarker but not a predictive biomarker of standard-of-care chemotherapy.

Indexed as

Carcinoma, Pancreatic DuctalGATA6 Transcription FactorGene AmplificationMutationPancreatic NeoplasmsTumor Suppressor Protein p53AgedAged, 80 and overBiomarkers, TumorFemaleHumansMaleMiddle AgedPrognosisProgression-Free SurvivalRetrospective StudiesBiomarkers, TumorGATA6 protein, humanGATA6 Transcription FactorTP53 protein, humanTumor Suppressor Protein p53human organoidspancreatic cancerpancreatic ductal adenocarcinomaprognostic biomarker

Identifiers

PMID40262102
PMCPMC12143463

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Registered trials

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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.