Evidence map›Paper›PMID 29766388›Full record

ReviewDigestive diseases and sciences2018

Molecular Evolution of Metaplasia to Adenocarcinoma in the Esophagus.

William M Grady, Ming Yu

Open access · greenAbstract readReview
In one paragraph

Review in Digestive diseases and sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Intestinal metaplasia of the urinary tract harbors potentially oncogenic genetic variants.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. The role ofInfectious agents and cancer · 2019
    Review
  10. Article
  11. Article
  12. Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association
    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

2 authors at 1 institution in 1 country.

William M GradyClinical Research Division, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N. D4-100, Seattle, WA, 98109, USA. wgrady@fredhutch.org.
Ming YuClinical Research Division, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N. D4-100, Seattle, WA, 98109, USA.
Fred Hutch Cancer Center · US

Funding

Translational Bioimaging Core Shared ResourceP30CA015704 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Marian Esvelt · 1985 to 2026
$296.4M
Tumor mutation signaturesP01CA077852 · NCI · UNIVERSITY OF WASHINGTON · PI MONNAT, RAYMOND J · 1999 to 2019
$26.0M
Whole Exome Approaches for Esophageal Adenocarcinoma Susceptibility GenesU54CA163060 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI CHAK, AMITABH, GUDA, KISHORE · 2011 to 2022
$14.0M
Trans-NetworkU54CA143862 · NCI · ARIZONA STATE UNIVERSITY-TEMPE CAMPUS · PI MELDRUM, DEIRDRE R. · 2009 to 2013
$8.4M
Identify and validate novel epigenetic molecular markers for colorectal neoplasmU01CA152756 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GRADY, WILLIAM MALLORY, GUDA, KISHORE · 2010 to 2021
$6.7M
(PQ6) Radiogenomics of colorectal polyps to assess benign proliferative vs. premalignant states.R01CA220004 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GRADY, WILLIAM MALLORY, HALBERG, RICHARD BROTT · 2017 to 2021
$3.2M
TGF-beta signaling and colon cancerR01CA115513 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GRADY, WILLIAM MALLORY · 2007 to 2011
$1.6M
(PQC1) Accelerated biological aging and colon polyp to cancer progressionR01CA194663 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GRADY, WILLIAM MALLORY · 2015 to 2018
$1.6M
NCI NIH HHS P01 CA077852NCI NIH HHS P30 CA015704NCI NIH HHS R01 CA115513NCI NIH HHS R01 CA194663NCI NIH HHS R01 CA220004NCI NIH HHS U01 CA152756NCI NIH HHS U54 CA143862NCI NIH HHS U54 CA163060
6 · The paper itself

Abstract

Esophageal adenocarcinoma (EAC) develops from Barrett's esophagus (BE), a condition where the normal squamous epithelia is replaced by specialized intestinal metaplasia in response to chronic gastroesophageal acid reflux. In a minority of individuals, BE can progress to low- and high-grade dysplasia and eventually to intra-mucosal and then invasive carcinoma. BE provides researchers with a unique model to characterize the process by which a carcinoma arises from its precursor lesion. Molecular studies of BE have demonstrated that it is not simply a metaplastic tissue, but rather it harbors frequent alterations that are also present in dysplastic BE and in EAC. Both BE and EAC are characterized by loss of heterozygosity, aneuploidy, specific genetic mutations, and clonal diversity. Epigenetic abnormalities, primary alterations in DNA methylation, are also frequently seen in BE and EAC. Candidate gene and array-based approaches have demonstrated that numerous tumor suppressor genes exhibit aberrant promoter methylation, and some of these altered genes are associated with the neoplastic progression of BE. It has also been shown that the BE and EAC epigenomes are characterized by hypomethylation of intragenic and non-coding regions Recent studies have also provided new insight into the evolutionary forces underlying the molecular alterations seen in BE and EAC and into the molecular pathogenesis of EAC.

Indexed as

Evolution, MolecularAdenocarcinomaBarrett EsophagusBiomarkers, TumorEpigenesis, GeneticEsophageal NeoplasmsEsophagusHumansMetaplasiaBiomarkers, TumorAneuploidyBarrett’s esophagusCancer genomicsDNA methylationEsophageal adenocarcinomaGenomic instabilityLOH

Identifiers

PMID29766388
PMCPMC6597264
OpenAlexW2804995446

What OpenQuestion holds

Textmetadata
LicenceTDM
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.