Evidence map›Paper›PMID 11034589›Full record

ArticleGut2000

Role of N-acetyltransferase polymorphisms in hepatitis B related hepatocellular carcinoma: impact of smoking on risk.

M W Yu, C I Pai, S Y Yang, T J Hsiao, H C Chang, S M Lin, Y F Liaw, P J Chen, C J Chen

Open access · hybridAbstract read
In one paragraph

Article in Gut, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Joint effect of polymorphism in the N-acetyltransferase 2 gene and smoking on hepatocellular carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. NAT1 polymorphisms and cancer risk: a systematic review and meta-analysis.International journal of clinical and experimental medicine · 2015
    Article
  7. Article
  8. Article
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  12. Article
  13. Epidemiology of primary and secondary liver cancers.Seminars in interventional radiology · 2006
    Article
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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 3 institutions in 1 country.

M W YuGraduate Institute of Epidemiology, College of Public Health, National Taiwan University, Taipei, Taiwan. mingwhei@ha.mc.ntu.edu.tw
C I Pai
S Y Yang
T J Hsiao
H C Chang
S M Lin
Y F Liaw
P J Chen
C J Chen
Chang Gung University · TWNational Taiwan University Hospital · TWNational Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPersistent infection with hepatitis B virus (HBV) causes chronic phasic necroinflammation and regenerative proliferation in the liver. The sustained hepatocellular proliferation may render chronic HBV carriers more susceptible to the effects of environmental carcinogens. Aromatic amines are potential hepatocarcinogens in humans. N-acetyltransferase (NAT) is involved in the metabolic activation and detoxification of these compounds.

aimsTo investigate if genetic polymorphisms in N-acetylation are related to hepatocellular carcinoma (HCC) among chronic HBV carriers.

methodsGenotyping of NAT1 and NAT2 was performed using polymerase chain reaction-restriction fragment length polymorphism on peripheral leucocyte DNA from 151 incident cases of HCC and 211 controls. All subjects were male, and were chronic HBV surface antigen carriers.

resultsA significant association between NAT2 genetic polymorphism and HCC was observed among chronic HBV carriers who were smokers but not among those who were non-smokers. For smoking HBV carriers, the odds ratios of developing HCC for those heterozygous and homozygous for the NAT2*4 functional allele compared with those without any copies of the functional allele (reference group) were 2.67 (95% confidence interval 1.15-6.22) and 2.58 (95% confidence interval 1.04-6.43), respectively. The interaction between cigarette smoking and the presence of the NAT2*4 allele just failed to reach statistical significance (p=0.06). No association between NAT1 genotype and HCC was evident overall or within the smoking stratified subgroups.

conclusionsOur results suggest that NAT2 activity may be particularly critical in smoking related hepatocarcinogenesis among chronic HBV carriers. Our data also indirectly support a role for tobacco smoke derived aromatic amines in the aetiology of HCC.

Indexed as

Polymorphism, Restriction Fragment LengthAcetyltransferasesAdultAgedAllelesCarcinoma, HepatocellularCase-Control StudiesGenotypeHepatitis B, ChronicHumansLeukocytesLiver NeoplasmsMaleMiddle AgedOdds RatioPolymerase Chain ReactionAcetyltransferases

Identifiers

PMID11034589
PMCPMC1728099
OpenAlexW2111604012

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.