Evidence map›Paper›PMID 36830789›Full record

ArticleBiomedicines2023

The Relationship between the Expression of GATA4 and GATA6 with the Clinical Characteristics and Prognosis of Resectable Pancreatic Adenocarcinoma.

Victoria Heredia-Soto, Laura Gutiérrez-Sainz, Ismael Ghanem, Laura Guerra, Elena Palacios, Marta de Uribe, Lucía Trilla-Fuertes, María de Miguel, Paloma Cejas, Laura Medina and 4 more

Open access · goldAbstract read
In one paragraph

Article in Biomedicines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

6 citing papers in PubMed, 9 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

14 authors at 4 institutions in 2 countries.

Victoria Heredia-SotoTranslational Oncology Research Laboratory, Biomedical Research Institute, La Paz University Hospital, IdiPAZ, Paseo de la Castellana 261, 28046 Madrid, Spain.
Laura Gutiérrez-SainzOncology Department, La Paz University Hospital, IdiPAZ, Paseo de la Castellana 261, 28046 Madrid, Spain.
Ismael GhanemOncology Department, La Paz University Hospital, IdiPAZ, Paseo de la Castellana 261, 28046 Madrid, Spain.ORCID 0000-0002-1859-0737
Laura GuerraPathology Department, La Paz University Hospital, Paseo de la Castellana 261, 28046 Madrid, Spain.
Elena PalaciosPathology Department, La Paz University Hospital, Paseo de la Castellana 261, 28046 Madrid, Spain.
Marta de UribePathology Department, La Paz University Hospital, Paseo de la Castellana 261, 28046 Madrid, Spain.
Lucía Trilla-FuertesMolecular Oncology Lab, Instituto de Genética Médica y Molecular-INGEMM, IdiPAZ, La Paz University Hospital, 28046 Madrid, Spain.ORCID 0000-0002-4452-3474
María de MiguelTranslational Oncology Research Laboratory, Biomedical Research Institute, La Paz University Hospital, IdiPAZ, Paseo de la Castellana 261, 28046 Madrid, Spain.
Paloma CejasTranslational Oncology Research Laboratory, Biomedical Research Institute, La Paz University Hospital, IdiPAZ, Paseo de la Castellana 261, 28046 Madrid, Spain.
Laura MedinaUGCI Medical Oncology Hospital Virgen de la Victoria, Instituto de Investigación Biomédica de Málaga, 29010 Málaga, Spain.ORCID 0000-0002-8041-3547
José Miguel CalderónPathology Department, Fuenlabrada University Hospital, 28942 Madrid, Spain.ORCID 0000-0003-0383-5639
David ViñalOncology Department, La Paz University Hospital, IdiPAZ, Paseo de la Castellana 261, 28046 Madrid, Spain.
Marta MendiolaTranslational Oncology Research Laboratory, Biomedical Research Institute, La Paz University Hospital, IdiPAZ, Paseo de la Castellana 261, 28046 Madrid, Spain.
Jaime FeliuOncology Department, La Paz University Hospital, IdiPAZ, Paseo de la Castellana 261, 28046 Madrid, Spain.ORCID 0000-0003-4867-1420
Hospital Universitario La Paz · ESDana-Farber Cancer Institute · USHospital Universitario de Fuenlabrada · ESInstituto de Investigación Biomédica de Málaga · ES

Funding

Instituto de Salud Carlos III PI18/01604
6 · The paper itself

Abstract

GATA4 and GATA6 are transcription factors involved in the differentiation and development of PDAC. GATA6 expression is related to the classic molecular subtype, while its absence is related to the basal-like molecular subtype. The aim was to determine the clinical utility of IHC determination of GATA4 and GATA6 in a series of patients with resected PDAC. GATA4 and GATA6 expression was studied by IHC in TMA samples of normal tissue, PanIN, tumor tissue and lymph node metastases from a series of 89 patients with resected PDAC. Its relationship with clinicopathologic variables and the outcome was investigated. Seventy-two (81%) tumors were GATA6+ and 37 (42%) were GATA4+. While GATA4 expression was reduced during tumor progression, GATA6 expression remained highly conserved, except in lymph node metastases. All patients with early stages and well-differentiated tumors were GATA6+. The absence of GATA4 expression was related to smoking. Patients with GATA4+ or GATA6+ tumors had significantly lower Ca 19.9 levels. The expression of GATA4 and GATA6 was related to DFS, being more favorable in the GATA4+/GATA6+ group. The determination of the expression of GATA4 and GATA6 by IHC is feasible and provides complementary clinical and prognostic information that can help improve the stratification of patients with PDAC.

Indexed as

carcinogenesisGATA4GATA6pancreatic ductal adenocarcinomaprognosticsurvival

Identifiers

PMID36830789
PMCPMC9953151
OpenAlexW4317433930

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.