Evidence map›Paper›PMID 22166497›Full record

ReviewCarcinogenesis2012

Current understanding of the mechanism of benzene-induced leukemia in humans: implications for risk assessment.

Cliona M McHale, Luoping Zhang, Martyn T Smith

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Carcinogenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
132citing papers in PubMed, 6 pooled it
4.6field-weighted citation impact, top 5% 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

132 citing papers in PubMed, 6 syntheses or guidelines pooled it, 333 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Environmental benzene exposure induces a conserved neutrophil degranulation program across species.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Article
  8. ALK Knock-In Reporter Reveals APE1 as a Negative Regulator ofInternational journal of molecular sciences · 2026
    Article
  9. Article
  10. Article
  11. Article
  12. Observational
  13. Review
  14. Article
  15. Smoking Aggravates Inflammation, Fibrogenesis, Angiogenesis and Cancer Risk in Patients With Cirrhosis.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Observational
  16. Article
  17. Review
  18. Cardiac abnormalities induced by benzene exposure from the flaring disaster at the BP refinery plant in Texas City.International journal of occupational medicine and environmental health · 2025
    Article
  19. A workflow for human health hazard evaluation using transcriptomic data and Key Characteristics-based gene sets.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Article
  20. Review

72 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Cliona M McHaleDivision of Environmental Health Sciences, Genes and Environment Laboratory, School of Public Health, University of California, Berkeley, CA 94720-7356, USA.
Luoping Zhang
Martyn T Smith
University of California, Berkeley · US

Funding

Training CoreP42ES004705 · NIEHS · UNIVERSITY OF CALIFORNIA BERKELEY · PI MORELLO-FROSCH, RACHEL ADELE · 1987 to 2025
$74.6M
NIEHS NIH HHS P42 ES004705NIEHS NIH HHS P42ES004705
6 · The paper itself

Abstract

Benzene causes acute myeloid leukemia and probably other hematological malignancies. As benzene also causes hematotoxicity even in workers exposed to levels below the US permissible occupational exposure limit of 1 part per million, further assessment of the health risks associated with its exposure, particularly at low levels, is needed. Here, we describe the probable mechanism by which benzene induces leukemia involving the targeting of critical genes and pathways through the induction of genetic, chromosomal or epigenetic abnormalities and genomic instability, in a hematopoietic stem cell (HSC); stromal cell dysregulation; apoptosis of HSCs and stromal cells and altered proliferation and differentiation of HSCs. These effects modulated by benzene-induced oxidative stress, aryl hydrocarbon receptor dysregulation and reduced immunosurveillance, lead to the generation of leukemic stem cells and subsequent clonal evolution to leukemia. A mode of action (MOA) approach to the risk assessment of benzene was recently proposed. This approach is limited, however, by the challenges of defining a simple stochastic MOA of benzene-induced leukemogenesis and of identifying relevant and quantifiable parameters associated with potential key events. An alternative risk assessment approach is the application of toxicogenomics and systems biology in human populations, animals and in vitro models of the HSC stem cell niche, exposed to a range of levels of benzene. These approaches will inform our understanding of the mechanisms of benzene toxicity and identify additional biomarkers of exposure, early effect and susceptibility useful for risk assessment.

Indexed as

AnimalsBenzeneHematopoietic Stem CellsHumansLeukemiaRisk AssessmentSystems BiologyToxicogeneticsBenzene

Identifiers

PMID22166497
PMCPMC3271273
OpenAlexW2139097852

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.