Evidence map›Paper›PMID 20625512›Full record

ArticlePloS one2010

Targeted deletion of Kcne2 causes gastritis cystica profunda and gastric neoplasia.

Torsten K Roepke, Kerry Purtell, Elizabeth C King, Krista M D La Perle, Daniel J Lerner, Geoffrey W Abbott

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

55 citing papers in PubMed, 76 citations in OpenAlex.

  1. Review
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  10. Review
  11. Article
  12. Article
  13. Article
  14. The Amyloid Precursor Protein C99 Fragment Modulates Voltage-Gated Potassium Channels.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2021
    Article
  15. Article
  16. Article
  17. Article
  18. Hypochlorhydria reduces mortality in heart failure caused by Kcne2 gene deletion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  19. Role of ion channels in gastrointestinal cancer.World journal of gastroenterology · 2019
    Review
  20. Analysis ofThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019
    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

6 authors at 2 institutions in 1 country.

Torsten K RoepkeDepartment of Pharmacology, Weill Medical College of Cornell University, New York, New York, United States of America.
Kerry Purtell
Elizabeth C King
Krista M D La Perle
Daniel J Lerner
Geoffrey W Abbott
Cornell University · USThe Ohio State University · US

Funding

K+ channel trafficking and modulation in MinK and MiRP1R01HL079275 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI ABBOTT, GEOFFREY W · 2005 to 2015
$4.6M
Predoctoral Training in Pharmacological SciencesT32GM073546 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI GROSS, STEVEN S · 2006 to 2020
$3.1M
NHLBI NIH HHS R01 HL079275NIGMS NIH HHS T32 GM073546
6 · The paper itself

Abstract

Gastric cancer is the second leading cause of cancer death worldwide. Predisposing factors include achlorhydria, Helicobacter pylori infection, oxyntic atrophy and TFF2-expressing metaplasia. In parietal cells, apical potassium channels comprising the KCNQ1 alpha subunit and the KCNE2 beta subunit provide a K(+) efflux current to facilitate gastric acid secretion by the apical H(+)K(+)ATPase. Accordingly, genetic deletion of murine Kcnq1 or Kcne2 impairs gastric acid secretion. Other evidence has suggested a role for KCNE2 in human gastric cancer cell proliferation, independent of its role in gastric acidification. Here, we demonstrate that 1-year-old Kcne2(-/-) mice in a pathogen-free environment all exhibit a severe gastric preneoplastic phenotype comprising gastritis cystica profunda, 6-fold increased stomach mass, increased Ki67 and nuclear Cyclin D1 expression, and TFF2- and cytokeratin 7-expressing metaplasia. Some Kcne2(-/-) mice also exhibited pyloric polypoid adenomas extending into the duodenum, and neoplastic invasion of thin walled vessels in the sub-mucosa. Finally, analysis of human gastric cancer tissue indicated reduced parietal cell KCNE2 expression. Together with previous findings, the results suggest KCNE2 disruption as a possible risk factor for gastric neoplasia.

Indexed as

AnimalsBlotting, WesternCell LineCell Line, TumorCyclin D1Fluorescent Antibody TechniqueGastric MucosaGastritisGene DeletionH(+)-K(+)-Exchanging ATPaseHumansImmunohistochemistryKCNQ1 Potassium ChannelKi-67 AntigenMetaplasiaMiceCyclin D1H(+)-K(+)-Exchanging ATPaseKCNE2 protein, humanKCNQ1 Potassium ChannelKCNQ1 protein, humanKi-67 AntigenPeptidesPotassium Channels, Voltage-GatedTFF2 protein, humanTrefoil Factor-2

Identifiers

PMID20625512
PMCPMC2897890
OpenAlexW2045774101

What OpenQuestion holds

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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.