Evidence map›Paper›PMID 19161591›Full record

ArticleJournal of experimental & clinical cancer research : CR2009

MUTYH Gln324His gene polymorphism and genetic susceptibility for lung cancer in a Japanese population.

Aiko Miyaishi, Kayo Osawa, Yasunori Osawa, Natsuko Inoue, Kana Yoshida, Mayumi Kasahara, Akimitsu Tsutou, Yoshiki Tabuchi, Kazuo Sakamoto, Noriaki Tsubota and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 11 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 11 pooled it
5.1field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 11 syntheses or guidelines pooled it, 63 citations in OpenAlex.

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  3. Smoking and hOGG1 Ser326Cys polymorphism contribute to lung cancer risk: evidence from a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
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  15. MUTYH: Not just polyposis.World journal of clinical oncology · 2020
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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

11 authors at 3 institutions in 1 country.

Aiko MiyaishiFaculty of Health Sciences, Kobe University Graduate School of Medicine, Kobe, Japan. m-stone@mtj.biglobe.ne.jp
Kayo Osawa
Yasunori Osawa
Natsuko Inoue
Kana Yoshida
Mayumi Kasahara
Akimitsu Tsutou
Yoshiki Tabuchi
Kazuo Sakamoto
Noriaki Tsubota
Juro Takahashi
Kobe University · JPHyogo Medical University · JPNishida Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGenetic polymorphisms of DNA repair enzymes in the base excision repair (BER) pathway, may lead to genetic instability and lung cancer carcinogenesis. We investigated the interactions among the gene polymorphisms in DNA repair genes and lung cancer.

methodsWe analyzed associations among OGG1 Ser326Cys and MUTYH Gln324His gene polymorphisms in relation to lung cancer risk using PCR-RFLP. The study involved 108 lung cancer patients and 121 non-cancer controls divided into non-smokers, smokers according to pack-years smoked in Japanese.

resultsThe results showed that the MUTYH His/His genotype compared with Gln/Gln genotype showed an increased risk for lung cancer (adjusted odds ratio [OR] 3.03, confidence interval [95%CI], 1.31-7.00, p = 0.010), whereas there was no significant increase for the Gln/His genotype (adjusted OR 1.35, 95%CI 0.70-2.61, p = 0.376). The MUTYH His/His genotype was at a borderline increased risk for both adenocarcinoma and squamous cell carcinoma (adjusted OR 2.50, 95%CI 0.95-6.62, p = 0.065 for adenocarcinoma; adjusted OR 3.20, 95%CI 0.89-11.49, p = 0.075 for squamous cell carcinoma, respectively). However, the OGG1 Ser/Cys or Cys/Cys genotypes compared with the Ser/Ser genotype did not have significantly increased risk for lung cancer, containing either adenocarcinoma or squamous cell carcinoma. The joint effect of tobacco exposure and the MUTYH His/His genotype compared with the Gln/Gln genotype showed a significant association with lung cancer risk in smokers, and there was not significantly increased in non-smokers (adjusted OR 3.82, 95%CI 1.22-12.00, p = 0.022 for smokers; adjusted OR 2.60, 95%CI 0.60-11.25, p = 0.200 for non-smokers, respectively). The effect of tobacco exposure and the OGG1 Ser326Cys showed also no significant risk for lung cancer.

conclusionOur findings suggest that the MUTYH Gln324His polymorphism appear to play an important role in modifying the risk for lung cancer in the Japanese population.

Indexed as

AdenocarcinomaAgedCarcinoma, Squamous CellCase-Control StudiesDNA GlycosylasesFemaleGenetic Predisposition to DiseaseHumansJapanLung NeoplasmsMaleMiddle AgedPolymorphism, GeneticRisk FactorsSmokingDNA GlycosylasesmutY adenine glycosylase

Identifiers

PMID19161591
PMCPMC2656466
OpenAlexW1978377168

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.