Evidence map›Paper›PMID 8968101›Full record

ArticleCancer research1996

Genotoxicity of aflatoxin B1: evidence for a recombination-mediated mechanism in Saccharomyces cerevisiae.

C Sengstag, B Weibel, M Fasullo

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Cancer research, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.3field-weighted citation impact, top 9% 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, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Genome Profiling for Aflatoxin BG3 (Bethesda, Md.) · 2020
    Article
  5. Article
  6. Article
  7. Activation of aflatoxin B1 by expression of human CYP1A2 polymorphisms in Saccharomyces cerevisiae.Mutation research. Genetic toxicology and environmental mutagenesis · 2014
    Article
  8. A single neonatal exposure to aflatoxin b1 induces prolonged genetic damage in two loci of mouse liver.Toxicological sciences : an official journal of the Society of Toxicology · 2012
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. CYP1B1 converts procarcinogens into genotoxins in Saccharomyces cerevisiae.Mutation research. Genetic toxicology and environmental mutagenesis
    Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

C SengstagGenetics Department, University of Zürich, Schwerzenbach, Switzerland.
B Weibel
M Fasullo
University of Zurich · CH

Funding

RADIATION INDUCTION OF GENOMIC REARRANGEMENTS IN YEASTR01CA070105 · NCI · ORDWAY RESEARCH INSTITUTE, INC. · PI FASULLO, MICHAEL THOMAS · 2000 to 2004
$1.1M
RADIATION INDUCTION OF GENOMIC REARRANGEMENTS IN YEASTR29CA070105 · NCI · LOYOLA UNIVERSITY CHICAGO · PI FASULLO, MICHAEL THOMAS · 1995 to 1999
–
NCI NIH HHS CA 70105NCI NIH HHS R01 CA070105NCI NIH HHS R29 CA070105
6 · The paper itself

Abstract

The potent liver carcinogen aflatoxin B1 (AFB1) is metabolized by cytochrome P450 to the mutagenic epoxide. We have observed that activated AFB1 also strongly induced mitotic recombination in the yeast Saccharomyces cerevisiae. To compare the recombinogenicity of AFB1 to its mutagenicity, three metabolically competent S. cerevisiae strains have been constructed. The frequencies of induced recombinants resulting from gene conversion or chromosomal translocations were determined by different prototrophic selections using two strains, whereas the inducibility of forward mutations was determined by the frequency of drug resistance in the third strain. Human cytochrome P4501A1- (CYP1A) and NADPH-cytochrome P450-oxidoreductase cDNAs were expressed in the strains to ensure intracellular metabolism to the epoxide. Exposure of the strains to AFB1 resulted in a 139- and 24-fold increase in the translocation and gene conversion frequencies, respectively, whereas the mutation frequency was increased only 3-fold. In contrast, benzo[a]pyrene-7,8-dihydrodiol and ethyl methanesulfonate induced mutation and mitotic recombination to similar degrees. We conclude that AFB1 exerted a strong recombinogenic, but only a weak mutagenic, effect. The recombinogenicity of AFB1 in yeast may indicate a mechanism for the high proportion of loss of heterozygosity that has been detected in AFB1-related human liver cancers.

Indexed as

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxideAflatoxin B1BiotransformationCarcinogensChromosomes, FungalCytochrome P-450 CYP1A1DNA, ComplementaryDNA, FungalGene ConversionHumansMutagenicity TestsMutagensNADPH-Ferrihemoprotein ReductaseRecombinant Fusion ProteinsRecombination, GeneticSaccharomyces cerevisiae7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxideAflatoxin B1CarcinogensCytochrome P-450 CYP1A1DNA, ComplementaryDNA, FungalMutagensNADPH-Ferrihemoprotein ReductaseRecombinant Fusion Proteins

Identifiers

PMID8968101
PMCPMC10195021
OpenAlexW1553421524

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.