Evidence map›Paper›PMID 21203850›Full record

ArticleMolecular biology reports2011

Copy number variations of chromosome 17p13.1 might be linked to high risk of lung cancer in heavy smokers.

Minhyeok Lee, Yeiwon Lee, Hyun-Jung Cho, Jeeyoung Hong, Sun-Jung Kwon, Chang-Gyo Park, Hoi-Young Lee, Ji-Woong Son, Jaeku Kang

Abstract read
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In one paragraph

Article in Molecular biology reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 29% 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

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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

4 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Minhyeok LeeMyunggok Medical Research Institute, College of Medicine, Konyang University, Daejeon 302-718, Republic of Korea.
Yeiwon Lee
Hyun-Jung Cho
Jeeyoung Hong
Sun-Jung Kwon
Chang-Gyo Park
Hoi-Young Lee
Ji-Woong Son
Jaeku Kang
Konyang University · KRKonyang University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the most common cause of cancer death worldwide. Smoking is known as the strongest single factor in the development of lung cancer. However, there are inherited genetic factors that cause different responses to cigarette smoking exposure among individuals. We tried to identify these differences in heavy smokers by examining copy number variations (CNVs) between lung cancer patients and healthy controls. Analysis by array comparative genomic hybridization which was tested with 20-person training set (10 lung cancer patients, 10 healthy controls) showed 26 significant (adjusted P < 0.05) clones with either copy number gains or losses. Three genes, KCTD11, FGF11, and PTPRH on chromosomal regions 17p13.1 (KCTD11 and FGF11) and 19q13.42 (PTPRH), were selected (adjusted P < 0.001) and tested by real-time quantitative PCR with 34 healthy controls and 54 lung cancer patients. KCTD11 on the chromosomal region 17p13.1 showed significant high odds ratio (OR = 16.0) in heavy smokers, implying that this is a susceptibility region for lung cancer in this group. Therefore, CNVs of 17p13.1 is a promising candidate to identify individuals with a high genetic risk for the development of lung cancer.

Indexed as

Genetic Predisposition to DiseaseCase-Control StudiesCell Line, TumorChromosomes, Human, Pair 17Cluster AnalysisComparative Genomic HybridizationDNA Copy Number VariationsGene Expression Regulation, NeoplasticGene FrequencyHumansLung NeoplasmsOdds RatioReal-Time Polymerase Chain ReactionRisk FactorsRNA, MessengerSmokingRNA, Messenger

Identifiers

PMID21203850
OpenAlexW1975594259

What OpenQuestion holds

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Registered trials

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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.