Evidence map›Paper›PMID 34069279›Full record

ReviewCancers2021

Epigenetic Effects of Benzene in Hematologic Neoplasms: The Altered Gene Expression.

Giovanna Spatari, Alessandro Allegra, Mariella Carrieri, Giovanni Pioggia, Sebastiano Gangemi

Abstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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, 2 syntheses or guidelines pooled it.

  1. Occupational benzene exposure and risk of kidney and bladder cancers: a systematic review and meta-analysis.European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) · 2025
    Pooled it
  2. Recent Advances in Biomonitoring of Gas Station Workers: A Systematic Review.Asian Pacific journal of cancer prevention : APJCP · 2024
    Pooled it
  3. Article
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  13. Coexistence ofTranslational cancer research · 2023
    Article
  14. Review
  15. Therapy-Related Myeloid Neoplasms: Predisposition and Clonal Evolution.Mediterranean journal of hematology and infectious diseases · 2023
    Review
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  17. Article
  18. 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

5 authors.

Giovanna SpatariDepartment of Biomedical and Dentistry Sciences and Morphological and Functional Imaging, University of Messina, 98125 Messina, Italy.
Alessandro AllegraDivision of Hematology, Department of Human Pathology in Adulthood and Childhood "Gaetano Barresi", University of Messina, 98125 Messina, Italy.ORCID 0000-0001-6156-8239
Mariella CarrieriDepartment of Cardiac Thoracic Vascular Sciences and Public Health, University of Padova, 35128 Padova, Italy.
Giovanni PioggiaInstitute for Biomedical Research and Innovation (IRIB), National Research Council of Italy (CNR), 98164 Messina, Italy.ORCID 0000-0002-8089-7449
Sebastiano GangemiSchool of Allergy and Clinical Immunology, Department of Clinical and Experimental Medicine, University of Messina, 98125 Messina, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Benzene carcinogenic ability has been reported, and chronic exposure to benzene can be one of the risk elements for solid cancers and hematological neoplasms. Benzene is acknowledged as a myelotoxin, and it is able to augment the risk for the onset of acute myeloid leukemia, myelodysplastic syndromes, aplastic anemia, and lymphomas. Possible mechanisms of benzene initiation of hematological tumors have been identified, as a genotoxic effect, an action on oxidative stress and inflammation and the provocation of immunosuppression. However, it is becoming evident that genetic alterations and the other causes are insufficient to fully justify several phenomena that influence the onset of hematologic malignancies. Acquired epigenetic alterations may participate with benzene leukemogenesis, as benzene may affect nuclear receptors, and provoke post-translational alterations at the protein level, thereby touching the function of regulatory proteins, comprising oncoproteins and tumor suppressor proteins. DNA hypomethylation correlates with stimulation of oncogenes, while the hypermethylation of CpG islands in promoter regions of specific tumor suppressor genes inhibits their transcription and stimulates the onset of tumors. The discovery of the systems of epigenetic induction of benzene-caused hematological tumors has allowed the possibility to operate with pharmacological interventions able of stopping or overturning the negative effects of benzene.

Indexed as

air pollutionbenzenecancerepigeneticgene expressionhematological malignanciesleukemialymphomaoccupational disease

Identifiers

PMID34069279
PMCPMC8156840

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.