Evidence map›Paper›PMID 21432264›Full record

ArticleEnvironmental health and preventive medicine2002

Genetic polymorphism of enzymes involved in xenobiotic metabolism and the risk of lung cancer.

Chikako Kiyohara, Taro Shirakawa, Julian M Hopkin

Open access · bronzeAbstract read
In one paragraph

Article in Environmental health and preventive medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 3 pooled it
1.4field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 3 syntheses or guidelines pooled it, 36 citations in OpenAlex.

  1. The interaction between smoking and GSTM1 variant on lung cancer in the Chinese population.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Pooled it
  2. Pooled it
  3. NQO1, MPO, and the risk of lung cancer: a HuGE review.Genetics in medicine : official journal of the American College of Medical Genetics · 2005
    Pooled it
  4. Article
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  7. OncoTargets and therapy · 2017
    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

3 authors at 2 institutions in 2 countries.

Chikako KiyoharaDepartment of Preventive Medicine, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-Ku, 812-8582, Fukuoka, Japan, chikako@phealth.med.kyushu-u.ac.jp.
Taro Shirakawa
Julian M Hopkin
Kyoto University · JPSwansea University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inhalation of cigarette smoke is a major risk factor for the development of lung cancer. It has been suggested that genetic susceptibility may contribute to the risk, because only a small portion of smokers develops the disease. Several polymorphisms that involve the metabolic activation or detoxification of carcinogens derived from cigarette smoke have been found to be associated with lung cancer risk. Many studies have focused on the relation between the distribution of polymorphic variants of different forms of the metabolic enzymes and lung cancer susceptibility. In this respect two groups of genetic polymorphisms of enzymes involved in xenobiotic metabolism, cytochrome P450 (CYP) and glutathione S-transferases (GSTs), have been discussed.CYP multigene superfamily consists of 10 subfamilies (CYP1-CYP10). A positive association between development of lung cancer and the mutant homozygous genotype ofCYP1A1 gene has been reported in several Japanese populations but such an association has not been observed in either Caucasians or African-Americans. The relation betweenCYP2D6 and lung cancer remains conflicting and inconclusive. Several polymorphisms have been identified at theCYP2E1 locus. No definitive link between the polymorphisms ofCYP2E1 and the risk of lung cancer has, however, been identified. The role of otherCYP2 isoforms in lung carcinogenesis has not been sufficiently investigated.GSTs form a superfamily of genes consisting of five distinct families, namedGSTA, GSTM, GSTP, GSTT andGSTS. The role ofGSTM, GSTT1 orGSTP1 polymorphism in modifying the lung cancer risk may be more limited than has been so far anticipated.Although some genetic polymorphisms discussed here have not shown significant increases/decreases in risk, individuals with differing genotypes may have different susceptibilities to lung cancer. Hopefully, in future studies it will be possible to screen for lung cancer using specific biomarkers.

Indexed as

drug-metabolizing enzymesethnic differencegenetic polymorphismlung cancermolecular epidemiology

Identifiers

PMID21432264
PMCPMC2723399
OpenAlexW2080655793

What OpenQuestion holds

Textmetadata
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.