Evidence map›Paper›PMID 22675488›Full record

ArticlePloS one2012

Aflatoxin-induced TP53 R249S mutation in hepatocellular carcinoma in Thailand: association with tumors developing in the absence of liver cirrhosis.

Stephanie Villar, Sandra Ortiz-Cuaran, Behnoush Abedi-Ardekani, Doriane Gouas, Andre Nogueira da Costa, Amelie Plymoth, Thiravud Khuhaprema, Anant Kalalak, Suleeporn Sangrajrang, Marlin D Friesen and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Review
  3. Can We Interpret Analyses of Etiologic Heterogeneity When Molecular Markers Are Used to Classify Tumors?Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Hepatocellular carcinoma: old friends and new tricks.Experimental & molecular medicine · 2020
    Review
  8. Chemical Risk Factors of Primary Liver Cancer: An Update.Hepatic medicine : evidence and research · 2020
    Review
  9. Wild type p53 function in p53Journal of experimental & clinical cancer research : CR · 2019
    Article
  10. Liquid biopsies for hepatocellular carcinoma.Translational research : the journal of laboratory and clinical medicine · 2018
    Review
  11. Article
  12. Article
  13. Article
  14. Mutational spectra of aflatoxin BProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

12 authors at 4 institutions in 4 countries.

Stephanie VillarInternational Agency for Research on Cancer, Lyon, France.
Sandra Ortiz-Cuaran
Behnoush Abedi-Ardekani
Doriane Gouas
Andre Nogueira da Costa
Amelie Plymoth
Thiravud Khuhaprema
Anant Kalalak
Suleeporn Sangrajrang
Marlin D Friesen
John D Groopman
Pierre Hainaut
Centre International de Recherche sur le Cancer · FRNational Cancer Institute of Thailand · THJohns Hopkins University · USKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary Liver Cancer (PLC) is the leading cause of death by cancer among males in Thailand and the 3(rd) among females. Most cases are hepatocellular carcinoma (HCC) but cholangiocarcinomas represent between 4 and 80% of liver cancers depending upon geographic area. Most HCC are associated with chronic infection by Hepatitis B Virus while a G → T mutation at codon 249 of the TP53 gene, R249S, specific for exposure to aflatoxin, is detected in tumors for up to 30% of cases. We have used Short Oligonucleotide Mass Analysis (SOMA) to quantify free circulating R249S-mutated DNA in plasma using blood specimens collected in a hospital case:control study. Plasma R249S-mutated DNA was detectable at low concentrations (≥ 67 copies/mL) in 53 to 64% of patients with primary liver cancer or chronic liver disease and in 19% of controls. 44% of patients with HCC and no evidence of cirrhosis had plasma concentrations of R249S-mutated DNA ≥ 150 copies/mL, compared to 21% in patients with both HCC and cirrhosis, 22% in patients with cholangiocarcinoma, 12% in patients with non-cancer chronic liver disease and 3% of subjects in the reference group. Thus, plasma concentrations of R249S-mutated DNA ≥ 150 copies/mL tended to be more common in patients with HCC developing without pre-existing cirrhosis (p = 0.027). Overall, these results support the preferential occurrence of R249S-mutated DNA in HCC developing in the absence of cirrhosis in a context of HBV chronic infection.

Indexed as

AdultAflatoxinsAgedalpha-FetoproteinsAmino Acid SubstitutionCarcinoma, HepatocellularCell Transformation, NeoplasticDNA, NeoplasmFemaleGeographyHepatitis B Surface AntigensHepatitis C AntibodiesHepatitis, ChronicHumansLiver CirrhosisLiver NeoplasmsAflatoxinsalpha-FetoproteinsDNA, NeoplasmHepatitis B Surface AntigensHepatitis C AntibodiesTumor Suppressor Protein p53

Identifiers

PMID22675488
PMCPMC3366967
OpenAlexW2035480088

What OpenQuestion holds

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LicenceCC BY
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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.