Evidence map›Paper›PMID 8659516›Full record

ArticleAmerican journal of human genetics1996

Chronic hepatitis B carriers with null genotypes of glutathione S-transferase M1 and T1 polymorphisms who are exposed to aflatoxin are at increased risk of hepatocellular carcinoma.

C J Chen, M W Yu, Y F Liaw, L W Wang, S Chiamprasert, F Matin, A Hirvonen, D A Bell, R M Santella

Open access · greenAbstract read
In one paragraph

Article in American journal of human genetics, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 4 pooled it
1.8field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 4 syntheses or guidelines pooled it, 110 citations in OpenAlex.

  1. Quantitative assessment of the effect of glutathione S-transferase genes GSTM1 and GSTT1 on hepatocellular carcinoma risk.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Review
  6. Chronic and Acute Toxicities of Aflatoxins: Mechanisms of Action.International journal of environmental research and public health · 2020
    Review
  7. Environmental Exposures and Hepatocellular Carcinoma.Journal of clinical and translational hepatology · 2013
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Pharmacogenomics: a tool for improving cancer chemotherapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2008
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. 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

9 authors at 1 institution in 1 country.

C J ChenInstitute of Epidemiology, College of Public Health, National Taiwan University, Taiwan.
M W Yu
Y F Liaw
L W Wang
S Chiamprasert
F Matin
A Hirvonen
D A Bell
R M Santella
National Taiwan University · TW

Funding

BIOLOGICAL MONITORING FOR EXPOSURE TO AFLATOXINR01ES005116 · NIEHS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI SANTELLA, REGINA M · 1990 to 2014
$5.2M
NIEHS NIH HHS ES05116NIEHS NIH HHS R01 ES005116
6 · The paper itself

Abstract

This study was carried out to elucidate the effect of glutathione S-transferase (GST) Ml and Tl polymorphisms on the aflatoxin-related hepatocarcinogenesis among chronic carriers of hepatitis B surface antigen (HBsAg). A total of 32 newly diagnosed hepatocellular carcinoma (HCC) cases and 73 age-matched controls selected from a cohort of 4,841 chronic HBsAg carriers who had been followed for 5 years were studied. The level of aflatoxin B1 (AFB1)-albumin adducts in their serum samples collected at the recruitment was examined by competitive enzyme-linked immunosorbance assay, and genotypes of GST M1 and T1 were determined by PCR. There was a dose-response relationship between serum level of AFB1-albumin adducts and risk of HCC. The biological gradients between serum AFB1-albumin adducts level and HCC risk were observed among chronic HBsAg carriers who had null genotypes of GST M1 and/or T1 but not among those who had non-null genotypes. The multivariate-adjusted odds ratios of developing HCC for those who had low and high serum levels of AFB1-albumin adducts compared with those who had a undetectable adduct level as the referent (odds ratio = 1.0) were 4.1 and 12.4, respectively, for HBsAg carriers with null GST M1 genotype (P < .01, on the basis of the significance test for trend); 0.7 and 1.4 for those with non-null GST Ml genotype (P = .98); 1.8 and 10.2 for those with null GST T1 genotype (P < .05); and 1.3 and 0.8 for those with non-null GST T1 genotype (P = .93). The interaction between serum AFB1-albumin adduct level and polymorphisms of GST M1 and T1 was at marginal statistical significance levels (.05 < P < .10).

Indexed as

Carrier StateAdultAflatoxin B1AflatoxinsAgedAlbuminsCarcinoma, HepatocellularCohort StudiesGenotypeGlutathione TransferaseHepatitis BHepatitis B Surface AntigensHumansLiver NeoplasmsMaleMiddle Agedaflatoxin-albumin adductAflatoxin B1AflatoxinsAlbuminsGlutathione TransferaseHepatitis B Surface Antigens

Identifiers

PMID8659516
PMCPMC1915093
OpenAlexW1561521870

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.