Evidence map›Paper›PMID 27325420›Full record

ArticleGut2017

GATA6 regulates EMT and tumour dissemination, and is a marker of response to adjuvant chemotherapy in pancreatic cancer.

Paola Martinelli, Enrique Carrillo-de Santa Pau, Trevor Cox, Bruno Sainz, Nelson Dusetti, William Greenhalf, Lorenzo Rinaldi, Eithne Costello, Paula Ghaneh, Núria Malats and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Gut, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 183 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
183citing papers in PubMed, 2 pooled it
8.2field-weighted citation impact, top 2% 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

183 citing papers in PubMed, 2 syntheses or guidelines pooled it, 270 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  11. GATA4 loss promotes mutantbioRxiv : the preprint server for biology · 2026
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123 more citing papers are in PubMed but not listed here.

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

16 authors at 10 institutions in 6 countries.

Paola MartinelliEpithelial Carcinogenesis Group, Spanish National Cancer Research Center-CNIO, Madrid, Spain.
Enrique Carrillo-de Santa PauEpithelial Carcinogenesis Group, Spanish National Cancer Research Center-CNIO, Madrid, Spain.
Trevor CoxCancer Research UK Liverpool Clinical Trials Unit, University of Liverpool, Liverpool, UK.
Bruno SainzDepartment of Preventive Medicine, Public Health and Microbiology, Universidad Autónoma de Madrid, Madrid, Spain.
Nelson DusettiCentre de Recherche en Cancérologie de Marseille (CRCM), INSERM U1068, CNRS UMR 7258, Aix-Marseille Université and Institut Paoli-Calmettes, Parc Scientifique et Technologique de Luminy, Marseille, France.
William GreenhalfNIHR Liverpool Pancreas Biomedical Research Unit, Department of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, UK.
Lorenzo RinaldiEpithelial Carcinogenesis Group, Spanish National Cancer Research Center-CNIO, Madrid, Spain.
Eithne CostelloCancer Research UK Liverpool Clinical Trials Unit, University of Liverpool, Liverpool, UK.
Paula GhanehCancer Research UK Liverpool Clinical Trials Unit, University of Liverpool, Liverpool, UK.
Núria MalatsGenetic and Molecular Epidemiology Group, Spanish National Cancer Research Center-CNIO, Madrid, Spain.
Markus BüchlerDepartment for General, Visceral and Transplantation Surgery, University Hospital Heidelberg, Heidelberg, Germany.
Marina PajicCancer Division, The Kinghorn Cancer Centre, Garvan Institute of Medical Research, Sydney, Australia.
Andrew V BiankinCancer Division, The Kinghorn Cancer Centre, Garvan Institute of Medical Research, Sydney, Australia.
Juan IovannaCentre de Recherche en Cancérologie de Marseille (CRCM), INSERM U1068, CNRS UMR 7258, Aix-Marseille Université and Institut Paoli-Calmettes, Parc Scientifique et Technologique de Luminy, Marseille, France.
John NeoptolemosCancer Research UK Liverpool Clinical Trials Unit, University of Liverpool, Liverpool, UK.
Francisco X RealEpithelial Carcinogenesis Group, Spanish National Cancer Research Center-CNIO, Madrid, Spain.
Spanish National Cancer Research Centre · ESCancer Research UK · GBNIHR Liverpool Pancreatic Biomedical Research Unit · GBAix-Marseille Université · FRCancer Australia · AUCentre de Recherche en Cancérologie de Marseille · FRHeidelberg University · DESouth Western Sydney Local Health District · AUUniversidad Autónoma de Madrid · ESUniversity of Liverpool · GB

Funding

Austrian Science Fund FWF P 27361Cancer Research UK 11883Cancer Research UK 15957Cancer Research UK 16186Cancer Research UK 16812Cancer Research UK 17263Cancer Research UK 17680Cancer Research UK 8968Chief Scientist Office SGP/1Department of Health 08/29/02Department of Health PB-PG-0407-13363Medical Research Council MC_PC_15080Medical Research Council MR/N005813/1Wellcome Trust
6 · The paper itself

Abstract

BACKGROUND AND

aimsThe role of GATA factors in cancer has gained increasing attention recently, but the function of GATA6 in pancreatic ductal adenocarcinoma (PDAC) is controversial. GATA6 is amplified in a subset of tumours and was proposed to be oncogenic, but high GATA6 levels are found in well-differentiated tumours and are associated with better patient outcome. By contrast, a tumour-suppressive function of GATA6 was demonstrated using genetic mouse models. We aimed at clarifying GATA6 function in PDAC.

designWe combined GATA6 silencing and overexpression in PDAC cell lines with GATA6 ChIP-Seq and RNA-Seq data, in order to understand the mechanism of GATA6 functions. We then confirmed some of our observations in primary patient samples, some of which were included in the ESPAC-3 randomised clinical trial for adjuvant therapy.

resultsGATA6 inhibits the epithelial-mesenchymal transition (EMT) in vitro and cell dissemination in vivo. GATA6 has a unique proepithelial and antimesenchymal function, and its transcriptional regulation is direct and implies, indirectly, the regulation of other transcription factors involved in EMT. GATA6 is lost in tumours, in association with altered differentiation and the acquisition of a basal-like molecular phenotype, consistent with an epithelial-to-epithelial (ET

conclusionsWe provide mechanistic insight into GATA6 tumour-suppressive function, its role as a regulator of canonical epithelial differentiation, and propose that loss of GATA6 expression is both prognostic and predictive of response to adjuvant therapy.

Indexed as

Carcinoma, Pancreatic DuctalGATA6 Transcription FactorPancreatic NeoplasmsAnimalsAntimetabolites, AntineoplasticCell Line, TumorCell MovementChemotherapy, AdjuvantEpithelial-Mesenchymal TransitionFluorouracilGene Expression Regulation, NeoplasticHumansMiceStatistics as TopicAntimetabolites, AntineoplasticFluorouracilGATA6 protein, humanGATA6 Transcription FactorADJUVANT TREATMENTCANCER GENETICSEPITHELIAL DIFFERENTIATIONGENE REGULATIONPANCREATIC CANCER

Identifiers

PMID27325420
PMCPMC5070637
OpenAlexW2470222015

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.