Evidence map›Paper›PMID 27731371›Full record

ArticleScientific reports2016

Transcriptional regulation by normal epithelium of premalignant to malignant progression in Barrett's esophagus.

Jia Zeng, Laimonas Kelbauskas, Aida Rezaie, Kristen Lee, Benjamin Ueberroth, Weimin Gao, Dmitry Derkach, Thai Tran, Dean Smith, Kimberly J Bussey and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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.

Jia ZengCenter for Biosignatures Discovery Automation, The Biodesign Institute, Arizona State University, P.O. Box 876501, Tempe, AZ 85287-6501, United States.
Laimonas KelbauskasCenter for Biosignatures Discovery Automation, The Biodesign Institute, Arizona State University, P.O. Box 876501, Tempe, AZ 85287-6501, United States.
Aida RezaieCenter for Biosignatures Discovery Automation, The Biodesign Institute, Arizona State University, P.O. Box 876501, Tempe, AZ 85287-6501, United States.
Kristen LeeCenter for Biosignatures Discovery Automation, The Biodesign Institute, Arizona State University, P.O. Box 876501, Tempe, AZ 85287-6501, United States.
Benjamin UeberrothCenter for Biosignatures Discovery Automation, The Biodesign Institute, Arizona State University, P.O. Box 876501, Tempe, AZ 85287-6501, United States.
Weimin GaoCenter for Biosignatures Discovery Automation, The Biodesign Institute, Arizona State University, P.O. Box 876501, Tempe, AZ 85287-6501, United States.
Dmitry DerkachCenter for Biosignatures Discovery Automation, The Biodesign Institute, Arizona State University, P.O. Box 876501, Tempe, AZ 85287-6501, United States.
Thai TranCenter for Biosignatures Discovery Automation, The Biodesign Institute, Arizona State University, P.O. Box 876501, Tempe, AZ 85287-6501, United States.
Dean SmithCenter for Biosignatures Discovery Automation, The Biodesign Institute, Arizona State University, P.O. Box 876501, Tempe, AZ 85287-6501, United States.
Kimberly J BusseyCenter for Biosignatures Discovery Automation, The Biodesign Institute, Arizona State University, P.O. Box 876501, Tempe, AZ 85287-6501, United States.
Deirdre R MeldrumCenter for Biosignatures Discovery Automation, The Biodesign Institute, Arizona State University, P.O. Box 876501, Tempe, AZ 85287-6501, United States.

Funding

CEGSTech: Integrated Biologically-Active MicrosystemsP50HG002360 · NHGRI · UNIVERSITY OF WASHINGTON · PI MELDRUM, DEIRDRE R. · 2001 to 2012
$37.8M
NHGRI NIH HHS P50 HG002360
6 · The paper itself

Abstract

In carcinogenesis, intercellular interactions within and between cell types are critical but remain poorly understood. We present a study on intercellular interactions between normal and premalignant epithelial cells and their functional relevance in the context of premalignant to malignant progression in Barrett's esophagus. Using whole transcriptome profiling we found that in the presence of normal epithelial cells, dysplastic cells but not normal cells, exhibit marked down-regulation of a number of key signaling pathways, including the transforming growth factor beta (TGFβ) and epithelial growth factor (EGF). Functional assays revealed both cell types showed repressed proliferation and significant changes in motility (speed, displacement and directionality) as a result of interactions between the two cell types. Cellular interactions appear to be mediated through both direct cell-cell contact and secreted ligands. The findings of this study are important in that they reveal, for the first time, the effects of cellular communication on gene expression and cellular function between premalignant (dysplastic) epithelial cells and their normal counterparts.

Indexed as

Gene Expression RegulationTranscription, GeneticBarrett EsophagusCell CommunicationCell LineCell Line, TumorCoculture TechniquesCulture Media, ConditionedDisease ProgressionEpidermal Growth FactorEpitheliumHumansSequence Analysis, RNATranscriptomeTransforming Growth Factor betaCulture Media, ConditionedEpidermal Growth FactorTransforming Growth Factor beta

Identifiers

PMID27731371
PMCPMC5059688

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.