Evidence map›Paper›PMID 33300112›Full record

ArticleJournal of cancer research and clinical oncology2021

GATA binding protein 6 (GATA6) is co-amplified with PIK3CA in patients with esophageal adenocarcinoma and is linked to neoadjuvant therapy.

Patrick Sven Plum, Heike Löser, Thomas Zander, Ahlem Essakly, Christiane J Bruns, Axel M Hillmer, Hakan Alakus, Wolfgang Schröder, Reinhard Büttner, Florian Gebauer and 1 more

Open access · hybridAbstract read
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In one paragraph

Article in Journal of cancer research and clinical oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 29% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

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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

11 authors at 2 institutions in 2 countries.

Patrick Sven PlumDepartment of General, Visceral, Cancer, and Transplantation Surgery, University of Cologne, Faculty of Medicine, and University Hospital Cologne, Kerpener Straße 62, 50937, Cologne, Germany. Patrick.plum@uk-koeln.de.ORCID http://orcid.org/0000-0002-8165-4553
Heike LöserGastrointestinal Cancer Group Cologne (GCGC), Cologne, Germany.
Thomas ZanderCentre for Integrated Oncology (CIO), Cologne Bonn, Cologne, Germany.
Ahlem EssaklyInstitute of Pathology, University of Cologne, Faculty of Medicine, and University Hospital Cologne, Kerpener Straße 62, 50937, Cologne, Germany.
Christiane J BrunsDepartment of General, Visceral, Cancer, and Transplantation Surgery, University of Cologne, Faculty of Medicine, and University Hospital Cologne, Kerpener Straße 62, 50937, Cologne, Germany.
Axel M HillmerInstitute of Pathology, University of Cologne, Faculty of Medicine, and University Hospital Cologne, Kerpener Straße 62, 50937, Cologne, Germany.
Hakan AlakusDepartment of General, Visceral, Cancer, and Transplantation Surgery, University of Cologne, Faculty of Medicine, and University Hospital Cologne, Kerpener Straße 62, 50937, Cologne, Germany.
Wolfgang SchröderDepartment of General, Visceral, Cancer, and Transplantation Surgery, University of Cologne, Faculty of Medicine, and University Hospital Cologne, Kerpener Straße 62, 50937, Cologne, Germany.
Reinhard BüttnerInstitute of Pathology, University of Cologne, Faculty of Medicine, and University Hospital Cologne, Kerpener Straße 62, 50937, Cologne, Germany.
Florian GebauerDepartment of General, Visceral, Cancer, and Transplantation Surgery, University of Cologne, Faculty of Medicine, and University Hospital Cologne, Kerpener Straße 62, 50937, Cologne, Germany.
Alexander QuaasGastrointestinal Cancer Group Cologne (GCGC), Cologne, Germany.
University of Cologne · DEUniversity Hospital Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeDriver mutations are typically absent in esophageal adenocarcinoma (EAC). Mostly, oncogenes are amplified as driving molecular events (including GATA6-amplification in 14% of cases). However, only little is known about its biological function and clinical relevance.

methodsWe examined a large number of EAC (n = 496) for their GATA6 amplification by fluorescence in situ hybridization (FISH) analyzing both primary resected (n = 219) and neoadjuvant treated EAC (n = 277). Results were correlated to clinicopathological data and known mutations/amplifications in our EAC-cohort.

resultsGATA6 amplification was detectable in 49 (9.9%) EACs of our cohort. We observed an enrichment of GATA6-positive tumors among patients after neoadjuvant treatment (12,3% amplified tumors versus 6,8% in the primary resected group; p = 0.044). Additionally, there was a simultaneous amplification of PIK3CA and GATA6 (p < 0.001) not detectable when analyzing other genes such as EGFR, ERBB2, KRAS or MDM2. Although we did not identify a survival difference depending on GATA6 in the entire cohort (p = 0.212), GATA6 amplification was associated with prolonged overall survival among patients with primary surgery (median overall-survival 121.1 vs. 41.4 months, p = 0.032). Multivariate cox-regression analysis did not confirm GATA6 as an independent prognostic marker, neither in the entire cohort (p = 0.210), nor in the subgroup with (p = 0.655) or without pretreatment (p = 0.961).

conclusionsOur study investigates the relevance of GATA6 amplification on a large tumor collective, which includes primary resected tumors and the clinically relevant group of neoadjuvant treated EACs. Especially in the pretreated group, we found an accumulation of GATA6-amplified tumors (12.3%) and a frequent co-amplification of PIK3CA. Our data suggest an increased resistance to radio-chemotherapy in GATA6-amplified tumors.

Indexed as

Gene AmplificationAdenocarcinomaAdultAgedAged, 80 and overClass I Phosphatidylinositol 3-KinasesEsophageal NeoplasmsFemaleFollow-Up StudiesGATA6 Transcription FactorHumansMaleMiddle AgedNeoadjuvant TherapyPrognosisRetrospective StudiesClass I Phosphatidylinositol 3-KinasesGATA6 protein, humanGATA6 Transcription FactorPIK3CA protein, humanBiomarkerEACEsophageal adenocarcinomaGATA6Neoadjuvant therapyNeoadjuvant treatmentPIK3CAPrognosisTreatment response

Identifiers

PMID33300112
PMCPMC7954758
OpenAlexW3111855205

What OpenQuestion holds

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LicenceCC BY
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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.