Evidence map›Paper›PMID 34227026›Full record

ArticleJournal of gastroenterology2021

Alteration of protein expression and spliceosome pathway activity during Barrett's carcinogenesis.

Christoph Stingl, Angela Bureo Gonzalez, Coşkun Güzel, Kai Yi Nadine Phoa, Michail Doukas, Gerben Eise Breimer, Sybren Lodewijk Meijer, Jacques Johannes Bergman, Theo Marten Luider

Open access · hybridAbstract read
In one paragraph

Article in Journal of gastroenterology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Exosomes in esophageal cancer: function and therapeutic prospects.Medical oncology (Northwood, London, England) · 2024
    Review
  3. 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

9 authors at 3 institutions in 1 country.

Christoph StinglDepartment of Neurology, Erasmus University Medical Center, PO Box 20440, 3000 CA, Rotterdam, The Netherlands. c.stingl@erasmusmc.nl.ORCID 0000-0002-3089-5373
Angela Bureo GonzalezDepartment of Gastroenterology and Hepatology, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Coşkun GüzelDepartment of Neurology, Erasmus University Medical Center, PO Box 20440, 3000 CA, Rotterdam, The Netherlands.
Kai Yi Nadine PhoaDepartment of Gastroenterology and Hepatology, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Michail DoukasDepartment of Pathology, Erasmus University Medical Center, Rotterdam, The Netherlands.
Gerben Eise BreimerDepartment of Pathology, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Sybren Lodewijk MeijerDepartment of Pathology, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Jacques Johannes BergmanDepartment of Gastroenterology and Hepatology, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Theo Marten LuiderDepartment of Neurology, Erasmus University Medical Center, PO Box 20440, 3000 CA, Rotterdam, The Netherlands.
Amsterdam University Medical Centers · NLErasmus MC · NLUniversity Medical Center Utrecht · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBarrett's esophagus (BE) is a known precursor lesion and the strongest risk factor for esophageal adenocarcinoma (EAC), a common and lethal type of cancer. Prediction of risk, the basis for efficient intervention, is commonly solely based on histologic examination. This approach is challenged by problems such as inter-observer variability in the face of the high heterogeneity of dysplastic tissue. Molecular markers might offer an additional way to understand the carcinogenesis and improve the diagnosis-and eventually treatment. In this study, we probed significant proteomic changes during dysplastic progression from BE into EAC.

methodsDuring endoscopic mucosa resection, epithelial and stromal tissue samples were collected by laser capture microdissection from 10 patients with normal BE and 13 patients with high-grade dysplastic/EAC. Samples were analyzed by mass spectrometry-based proteomic analysis. Expressed proteins were determined by label-free quantitation, and gene set enrichment was used to find differentially expressed pathways. The results were validated by immunohistochemistry for two selected key proteins (MSH6 and XPO5).

resultsComparing dysplastic/EAC to non-dysplastic BE, we found in equal volumes of epithelial tissue an overall up-regulation in terms of protein abundance and diversity, and determined a set of 226 differentially expressed proteins. Significantly higher expressions of MSH6 and XPO5 were validated orthogonally and confirmed by immunohistochemistry.

conclusionsOur results demonstrate that disease-related proteomic alterations can be determined by analyzing minute amounts of cell-type-specific collected tissue. Further analysis indicated that alterations of certain pathways associated with carcinogenesis, such as micro-RNA trafficking, DNA damage repair, and spliceosome activity, exist in dysplastic/EAC.

Indexed as

Barrett EsophagusDisease ProgressionEndoscopic Mucosal ResectionGene ExpressionHumansMicroRNAsNetherlandsSpliceosomesMicroRNAsAdenocarcinomaBarrett’s esophagusLaser capture microdissectionMass spectrometryProteomics

Identifiers

PMID34227026
PMCPMC8370908
OpenAlexW3182712914

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.