Evidence map›Paper›PMID 33507988›Full record

ArticlePloS one2021

Influence of single nucleotide polymorphisms among cigarette smoking and non-smoking patients with coronary artery disease, urinary bladder cancer and lung cancer.

Nongnit Laytragoon Lewin, Jan-Erik Karlsson, David Robinsson, Matida Fagerberg, Magnus Kentsson, Shariel Sayardoust, Mats Nilsson, Levar Shamoun, Bengt-Åke Andersson, Sture Löfgren and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2021. 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
1.3field-weighted citation impact, top 22% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Trial
  2. A Case Study on PPM1D and 9 Other Shared Germline Alterations in a Family.Asian Pacific journal of cancer prevention : APJCP · 2023
    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

12 authors at 2 institutions in 1 country.

Nongnit Laytragoon LewinDept Laboratory Medicine, Ryhov Hospital, Jönköping, Sweden.ORCID 0000-0001-6815-4530
Jan-Erik KarlssonDept of Internal Medicine, Ryhov Hospital, Jönköping, Sweden.ORCID 0000-0003-2632-4065
David RobinssonDept Urology, Ryhov Hospital, Jönköping, Sweden.ORCID 0000-0002-3433-8873
Matida FagerbergDept Urology, Ryhov Hospital, Jönköping, Sweden.
Magnus KentssonDept of Internal Medicine, Ryhov Hospital, Jönköping, Sweden.
Shariel SayardoustDept Periodontology, Ryhov Hospital, Jönköping, Sweden.
Mats NilssonFuturum, Academy of Health and Care, Region Jönköping, Jönköping, Sweden.
Levar ShamounDept Laboratory Medicine, Ryhov Hospital, Jönköping, Sweden.
Bengt-Åke AnderssonDept Laboratory Medicine, Ryhov Hospital, Jönköping, Sweden.
Sture LöfgrenDept Laboratory Medicine, Ryhov Hospital, Jönköping, Sweden.
Lars Erik RutqvistScientific Affairs Group, Swedish Match AB, Stockholm, Sweden.
Freddi LewinDept Oncology, Ryhov Hospital, Jönköping, Sweden.
Ryhov Hospital Jönköping · SELinköping University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionCigarette smoke is suggested to be a risk factor for coronary artery disease (CAD), urinary bladder cancer (UBCa) or lung cancer (LCa). However, not all heavy smokers develop these diseases and elevated cancer risk among first-degree relatives suggests an important role of genetic factor.

methodsThree hundred and ten healthy blood donors (controls), 98 CAD, 74 UBCa and 38 LCa patients were included in this pilot study. The influence of 92 single nucleotide polymorphisms (SNPs) and impact of cigarette smoking were analysed.

resultsOut of 92 SNPs tested, differences in distribution of 14 SNPs were detected between controls and patient groups. Only CTLA4 rs3087243 showed difference in both CAD and UBCa patient group compared to control group. Stratified by smoking status, the impact of smoking was associated to frequencies of 8, 3 and 4 SNPs in CAD, UBCa, LCa patients, respectively. None of these 92 SNPs showed a statistically significant difference to more than one type of disease among smoking patients. In non-smoking patients, 7, 3 and 6 SNPs were associated to CAD, UBCa, LCa, respectively. Out of these 92 SNPs, CTLA4 rs3087243 was associated to both non-smoking CAD and UBCa. The XRCC1 rs25487 was associated to both non-smoking UBCa and LCa.

conclusionSNPs might be important risk factors for CAD, UBCa and LCa. Distribution of the SNPs was specific for each patient group, not a random event. Impact of cigarette smoking on the disease was associated to the specific SNP sequences. Thus, smoking individuals with SNPs associated to risk of these serious diseases is an important target group for smoking cessation programs.

Indexed as

Genetic Predisposition to DiseaseAgedCase-Control StudiesCigarette SmokingCoronary Artery DiseaseFemaleHumansLung NeoplasmsMaleMiddle AgedPolymorphism, Single NucleotideUrinary Bladder Neoplasms

Identifiers

PMID33507988
PMCPMC7842923
OpenAlexW3122451039

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.