Evidence map›Paper›PMID 23300966›Full record

ArticlePloS one2013

The role of tobacco, alcohol, and obesity in neoplastic progression to esophageal adenocarcinoma: a prospective study of Barrett's esophagus.

Sheetal Hardikar, Lynn Onstad, Patricia L Blount, Robert D Odze, Brian J Reid, Thomas L Vaughan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 6 pooled it
12.2field-weighted citation impact, top 1% 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

50 citing papers in PubMed, 6 syntheses or guidelines pooled it, 99 citations in OpenAlex.

  1. Pooled it
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  4. Abnormal MGMT promoter methylation may contribute to the risk of esophageal cancer: a meta-analysis of cohort studies.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
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  6. Central adiposity is associated with increased risk of esophageal inflammation, metaplasia, and adenocarcinoma: a systematic review and meta-analysis.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2013
    Pooled it
  7. Trial
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  10. Article
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  17. Global burden and epidemiology of Barrett oesophagus and oesophageal cancer.Nature reviews. Gastroenterology & hepatology · 2021
    Review
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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 3 institutions in 1 country.

Sheetal HardikarPublic Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.
Lynn Onstad
Patricia L Blount
Robert D Odze
Brian J Reid
Thomas L Vaughan
University of Washington · USFred Hutch Cancer Center · USHarvard University · US

Funding

PHYLOGENIES of Barrett's Esophagus LineagesP01CA091955 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GRADY, WILLIAM MALLORY · 2002 to 2019
$35.9M
ESTABLISHED INVESTIGATOR AWARD IN CANCER PREVENTION AND CONTROLK05CA124911 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI VAUGHAN, THOMAS L · 2007 to 2016
$1.6M
NCI NIH HHS K05 CA124911NCI NIH HHS K05CA124911NCI NIH HHS P01 CA091955NCI NIH HHS P01CA091955
6 · The paper itself

Abstract

backgroundEsophageal adenocarcinoma (EA) incidence in many developed countries has increased dramatically over four decades, while survival remains poor. Persons with Barrett's esophagus (BE), who experience substantially elevated EA risk, are typically followed in surveillance involving periodic endoscopy with biopsies, although few progress to EA. No medical, surgical or lifestyle interventions have been proven to safely lower EA risk.

designWe investigated whether smoking, obesity or alcohol could predict progression to EA in a prospective cohort of 411 BE patients. Data were collected during personal interview. Adjusted hazard ratios (HR) were estimated using Cox regression.

results39% had body mass index (BMI) over 30 and 64% had smoked cigarettes. Main analyses focused on those with at least 5 months of follow-up (33,635 person-months), in whom 45 developed EA. Risk increased by 3% per year of age (trend p-value 0.02), with approximate doubling of risk among males. EA risk increased with smoking pack-years (trend p-value 0.04) and duration (p-value 0.05). Compared to never-smokers, the HR for those in the highest pack-year tertile was 2.29 (95%CI 1.04-5.07). No association was found with alcohol or BMI, whereas a suggestion of increased risk was observed in those with higher waist-hip ratio, especially among males.

conclusionEA risk significantly increased with increasing age and cigarette exposure. Abdominal obesity, but not BMI, was associated with a modest increased risk. Continued follow-up of this and other cohorts is needed to precisely define these relationships so as to inform risk stratification and preventive interventions.

Indexed as

AdenocarcinomaAdultAgedAlcohol DrinkingBarrett EsophagusBiopsyBody Mass IndexDisease ProgressionEsophageal NeoplasmsFemaleHumansLife StyleMaleMiddle AgedNicotianaObesity

Identifiers

PMID23300966
PMCPMC3536789
OpenAlexW2131887873

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.