Evidence map›Paper›PMID 27652669›Full record

ArticleEuropean biophysics journal : EBJ2016

In silico analysis of the transportome in human pancreatic ductal adenocarcinoma.

A Zaccagnino, C Pilarsky, D Tawfik, S Sebens, A Trauzold, I Novak, A Schwab, H Kalthoff

Abstract read
PubMed Publisher
In one paragraph

Article in European biophysics journal : EBJ, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.3field-weighted citation impact, top 31% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Identification of gastric cancer biomarkers throughBiochemistry and biophysics reports · 2024
    Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Transportome Malfunctions and the Hallmarks of Pancreatic Cancer.Reviews of physiology, biochemistry and pharmacology · 2021
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. 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

8 authors at 3 institutions in 2 countries.

A ZaccagninoInstitute for Experimental Cancer Research, Christian-Albrechts-University Kiel, UKSH, Campus Kiel, Arnold-Heller-Str. 3, 24105, Kiel, Germany. angela.zacca@email.uni-kiel.de.ORCID http://orcid.org/0000-0003-3972-7103
C PilarskyDepartment of Surgery, University Clinic, Krankenhausstr. 12, 91054, Erlangen, Germany.
D TawfikInstitute for Experimental Cancer Research, Christian-Albrechts-University Kiel, UKSH, Campus Kiel, Arnold-Heller-Str. 3, 24105, Kiel, Germany.
S SebensInstitute for Experimental Cancer Research, Christian-Albrechts-University Kiel, UKSH, Campus Kiel, Arnold-Heller-Str. 3, 24105, Kiel, Germany.
A TrauzoldInstitute for Experimental Cancer Research, Christian-Albrechts-University Kiel, UKSH, Campus Kiel, Arnold-Heller-Str. 3, 24105, Kiel, Germany.
I NovakSection for Cell Biology and Physiology, Department of Biology, Faculty of Science, University of Copenhagen, Universitetsparken 13, 2100, Copenhagen, Denmark.
A SchwabInstitute of Physiology II, University of Muenster, Robert-Koch-Str. 27 b, 48149, Muenster, Germany.
H KalthoffInstitute for Experimental Cancer Research, Christian-Albrechts-University Kiel, UKSH, Campus Kiel, Arnold-Heller-Str. 3, 24105, Kiel, Germany. holger.kalthoff@email.uni-kiel.de.
Christian-Albrechts-Universität zu Kiel · DEUniversitätsklinikum Erlangen · DEUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The altered expression and/or activity of ion channels and transporters (transportome) have been associated with malignant behavior of cancer cells and were proposed to be a hallmark of cancer. However, the impact of altered transportome in epithelial cancers, such as pancreatic ductal adenocarcinoma (PDAC), as well as its pathophysiological consequences, still remains unclear. Here, we report the in silico analysis of 840 transportome genes in PDAC patients' tissues. Our study was focused on the transportome changes and their correlation with functional and behavioral responses in PDAC tumor and stromal compartments. The dysregulated gene expression datasets were filtered using a cut-off of fold-change values ≤-2 or ≥2 (adjusted p value ≤0.05). The dysregulated transportome genes were clearly associated with impaired physiological secretory mechanisms and/or pH regulation, control of cell volume, and cell polarity. Additionally, some down-regulated transportome genes were found to be closely linked to epithelial cell differentiation. Furthermore, the observed decrease in genes coding for calcium and chloride transport might be a mechanism for evasion of apoptosis. In conclusion, the current work provides a comprehensive overview of the altered transportome expression and its association with predicted PDAC malignancy with special focus on the epithelial compartment.

Indexed as

Computational BiologyComputer SimulationGene Expression ProfilingAdenocarcinomaEpitheliumHumansIon ChannelsPancreatic NeoplasmsTumor MicroenvironmentIon ChannelsChronic pancreatitisGene expression analysisIon channelsPancreatic ductal adenocarcinomaTransportomeTumor stroma

Identifiers

PMID27652669
OpenAlexW2521749836

What OpenQuestion holds

Textmetadata
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.