Evidence map›Paper›PMID 34199909›Full record

ArticleCancers2021

Nrf2/Keap1-Pathway Activation and Reduced Susceptibility to Chemotherapy Treatment by Acidification in Esophageal Adenocarcinoma Cells.

Lucie Storz, Philipp Walther, Olga Chemnitzer, Orestis Lyros, Stefan Niebisch, Matthias Mehdorn, Boris Jansen-Winkeln, Yusef Moulla, Thomas Büch, Ines Gockel and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2021. 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
1.3field-weighted citation impact, top 21% 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, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Signaling pathways and their potential therapeutic utility in esophageal squamous cell carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
  6. 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

11 authors at 2 institutions in 1 country.

Lucie StorzDepartment of Visceral, Transplant, Thoracic and Vascular Surgery, University Hospital of Leipzig, Liebigstrasse 20, 04103 Leipzig, Germany.
Philipp WaltherDepartment of Visceral, Transplant, Thoracic and Vascular Surgery, University Hospital of Leipzig, Liebigstrasse 20, 04103 Leipzig, Germany.
Olga ChemnitzerDepartment of Visceral, Transplant, Thoracic and Vascular Surgery, University Hospital of Leipzig, Liebigstrasse 20, 04103 Leipzig, Germany.
Orestis LyrosDepartment of Visceral, Transplant, Thoracic and Vascular Surgery, University Hospital of Leipzig, Liebigstrasse 20, 04103 Leipzig, Germany.
Stefan NiebischDepartment of Visceral, Transplant, Thoracic and Vascular Surgery, University Hospital of Leipzig, Liebigstrasse 20, 04103 Leipzig, Germany.
Matthias MehdornDepartment of Visceral, Transplant, Thoracic and Vascular Surgery, University Hospital of Leipzig, Liebigstrasse 20, 04103 Leipzig, Germany.ORCID 0000-0002-0047-368X
Boris Jansen-WinkelnDepartment of Visceral, Transplant, Thoracic and Vascular Surgery, University Hospital of Leipzig, Liebigstrasse 20, 04103 Leipzig, Germany.ORCID 0000-0002-3996-9391
Yusef MoullaDepartment of Visceral, Transplant, Thoracic and Vascular Surgery, University Hospital of Leipzig, Liebigstrasse 20, 04103 Leipzig, Germany.
Thomas BüchMedical Faculty, Rudolf-Boehm-Institute for Pharmacology and Toxicology, Clinical Pharmacology, University of Leipzig, Haertelstrasse 16-18, 04103 Leipzig, Germany.
Ines GockelDepartment of Visceral, Transplant, Thoracic and Vascular Surgery, University Hospital of Leipzig, Liebigstrasse 20, 04103 Leipzig, Germany.
René ThiemeDepartment of Visceral, Transplant, Thoracic and Vascular Surgery, University Hospital of Leipzig, Liebigstrasse 20, 04103 Leipzig, Germany.ORCID 0000-0002-0537-3979
University Hospital Leipzig · DELeipzig University · DE

Funding

Barrett-Initiative e.V. Barrett-Initiative e.V.German Research Foundation (DFG) and Leipzig University program of Open Access PublishingMedizinische Fakultät, Universität Leipzig Clinical Scientist ProgramMedizinische Fakultät, Universität Leipzig Junior Research Grant
6 · The paper itself

Abstract

Chronic acid reflux causes cellular damage and inflammation in the lower esophagus. Due to these irritating insults, the squamous epithelium is replaced by metaplastic epithelium, which is a risk factor for the development of esophageal adenocarcinoma (EAC). In this study, we investigated the acid susceptibility in a Barrett's cell culture in vitro model, using six cell lines, derived from squamous epithelium (EPC1 and EPC2), metaplasia (CP-A), dysplasia (CP-B), and EAC (OE33 and OE19) cells. Cells exposed to acidic pH showed a decreased viability dependent on time, pH, and progression status in the Barrett's sequence, with the highest acid susceptibility in the squamous epithelium (EPC1 and EPC2), and the lowest in EAC cells. Acid pulsing was accompanied with an activation of the Nrf2/Keap1- and the NFκB-pathway, resulting in an increased expression of HO1-independent of the cellular context. OE33 showed a decreased responsiveness towards 5-FU, when the cells were grown in acidic conditions (pH 6 and pH 5.5). Our findings suggest a strong damage of squamous epithelium by gastroesophageal reflux, while Barrett's dysplasia and EAC cells apparently exert acid-protective features, which lead to a cellular resistance against acid reflux.

Indexed as

Barrett’s esophaguschemotherapyesophageal adenocarcinomagastroesophageal reflux disease (GERD)inflammation

Identifiers

PMID34199909
PMCPMC8200109
OpenAlexW3166652777

What Socratic 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 Socratic graph.