Evidence map›Paper›PMID 25478181›Full record

ArticleBMJ open respiratory research2014

Feasibility of using an epigenetic marker of risk for lung cancer, methylation of p16, to promote smoking cessation among US veterans.

Scott Shofer, Matthew Beyea, Sufeng Li, Lori A Bastian, Momen M Wahidi, Michael Kelley, Isaac M Lipkus

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in BMJ open respiratory research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01038492 (Testing the Feasibility of Using an Epigenetic Marker, p16, to Promote Smoking Cessation), which is not on this map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.3field-weighted citation impact, top 39% 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.

NCT01038492 nacompletednot on this map

Testing the Feasibility of Using an Epigenetic Marker, p16, to Promote Smoking Cessation

TypeinterventionalSponsorDuke UniversityRan2009 to 2010Enrolled35ConditionsTobacco Use Disorder, Smoking Cessation, Lung CancerArmsp16 Methylation and Lung Cancer Education
3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 3 citations in OpenAlex.

No citing paper in PubMed yet.

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

7 authors at 6 institutions in 1 country.

Scott ShoferPulmonary Section , Durham Veteran Affairs Medical Center , Durham, North Carolina , USA ; Division of Pulmonary, Allergy, and Critical Care , Duke University Medical Center , Durham, North Carolina , USA.
Matthew BeyeaPulmonx, Inc. , Redwood City, California , USA.
Sufeng LiDivision of Hematology/Oncology , Duke University Medical Center , Durham, North Carolina , USA.
Lori A BastianDepartment of Internal Medicine , Veteran Administration Connecticut Healthcare System , West Haven, Connecticut , USA ; Department of Internal Medicine , University of Connecticut Health Center , Farmington, Connecticut , USA.
Momen M WahidiDivision of Pulmonary, Allergy, and Critical Care , Duke University Medical Center , Durham, North Carolina , USA.
Michael KelleyDivision of Hematology/Oncology , Duke University Medical Center , Durham, North Carolina , USA ; Hematology and Oncology Section, Durham Veterans Affairs Medical Center, Durham, North Carolina , USA.
Isaac M LipkusDuke University School of Nursing , Durham, North Carolina , USA.
Durham VA Medical Center · USDuke Medical Center · USDuke University · USDuke University Hospital · USPulmonx (United States) · USUConn Health · US

Funding

RESEARCH BASE SUPPORT FOR COMMUNITY CLINICAL ONCOLOGY PRU10CA037447 · NCI · UNIVERSITY OF CHICAGO · PI BERTAGNOLLI, MONICA M, PASKETT, ELECTRA D. · 1985 to 2015
$25.3M
NCI NIH HHS U10 CA037447
6 · The paper itself

Abstract

introductionProviding smokers feedback using epigenetic markers of lung cancer risk has yet to be tested as a strategy to motivate smoking cessation. Epigenetic modification of Rb-p16 (p16) due to tobacco exposure is associated with increased risk of developing lung cancer. This study examined the acceptance of testing for methylated p16 and the understanding of test results in smokers at risk for development of lung cancer.

methodsThirty-five current smokers with airways obstruction viewed an educational presentation regarding p16 function followed by testing for the presence of methylated p16 in sputum. Participants were offered smoking cessation assistance and asked to complete surveys at the time of enrolment regarding their understanding of the educational material, perception of risk associated with smoking and desire to quit. Participants were notified of their test result and follow-up surveys were administered 2 and 10 weeks after notification of their test result.

resultsTwenty per cent of participants had methylated p16. Participants showed high degree of understanding of educational materials regarding the function and risk associated with p16 methylation. Sixty-seven per cent and 57% of participants with low-risk and high-risk test results, respectively, reported that the information was more likely to motivate them to quit smoking. Smoking cessation rates were similar between methylated and non-methylated participants.

conclusionsTesting for an epigenetic marker of lung cancer risk is accepted and understood by active smokers. A low-risk test result does not decrease motivation to stop smoking. TRIAL REGISTRATION NUMBER: NCT01038492.

Indexed as

Lung CancerTobacco and the lung

Identifiers

PMID25478181
PMCPMC4212704
OpenAlexW2165275921

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

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.