Evidence map›Paper›PMID 34274487›Full record

ReviewSeminars in cancer biology2021

Hexavalent chromium disrupts chromatin architecture.

Andrew VonHandorf, Hesbon A Zablon, Alvaro Puga

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

9 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Trivalent chromium interacts directly with acetylated lysine.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2025
    Article
  7. Review
  8. Article
  9. 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

3 authors at 2 institutions in 1 country.

Andrew VonHandorfDepartment of Environmental and Public Health Sciences and Center for Environmental Genetics, University of Cincinnati College of Medicine, 160 Panzeca Way, Cincinnati, OH, 45267, USA.
Hesbon A ZablonDepartment of Environmental and Public Health Sciences and Center for Environmental Genetics, University of Cincinnati College of Medicine, 160 Panzeca Way, Cincinnati, OH, 45267, USA.
Alvaro PugaDepartment of Environmental and Public Health Sciences and Center for Environmental Genetics, University of Cincinnati College of Medicine, 160 Panzeca Way, Cincinnati, OH, 45267, USA. Electronic address: Alvaro.Puga@uc.edu.
University of Cincinnati Medical Center · USUniversity of Cincinnati · US

Funding

REPRODUCTIVE AND DEVELOPMENTAL TOXICOLOGY RESEARCHP30ES006096 · NIEHS · UNIVERSITY OF CINCINNATI · PI PINNEY, SUSAN MENGEL · 1992 to 2022
$35.4M
ENVIRONMETAL CARCINOGENESIS AND MUTAGENESIST32ES007250 · NIEHS · UNIVERSITY OF CINCINNATI · PI MILLER, WILLIAM E · 1988 to 2024
$11.9M
MOLECULAR MECHANISMS OF COMPLEX MIXTURE TOXICITYR01ES010807 · NIEHS · UNIVERSITY OF CINCINNATI · PI PUGA, ALVARO · 2001 to 2021
$8.0M
NIEHS NIH HHS P30 ES006096NIEHS NIH HHS R01 ES010807NIEHS NIH HHS T32 ES007250
6 · The paper itself

Abstract

Accessibility of DNA elements and the orchestration of spatiotemporal chromatin-chromatin interactions are critical mechanisms in the regulation of gene transcription. Thus, in an ever-changing milieu, cells mount an adaptive response to environmental stimuli by modulating gene expression that is orchestrated by coordinated changes in chromatin architecture. Correspondingly, agents that alter chromatin structure directly impact transcriptional programs in cells. Heavy metals, including hexavalent chromium (Cr(VI)), are of special interest because of their ability to interact directly with cellular protein, DNA and other macromolecules, resulting in general damage or altered function. In this review we highlight the chromium-mediated mechanisms that promote disruption of chromatin architecture and how these processes are integral to its carcinogenic properties. Emerging evidence shows that Cr(VI) targets nucleosomal architecture in euchromatin, particularly in genomic locations flanking binding sites of the essential transcription factors CTCF and AP1. Ultimately, these changes contribute to an altered chromatin state in critical gene regulatory regions, which disrupts gene transcription in functionally relevant biological processes.

Indexed as

AnimalsCarcinogenesisChromatinChromiumHumansTranscription, GeneticChromatinChromiumchromium hexavalent ionChromatin architectureGene transcriptionHexavalent chromium

Identifiers

PMID34274487
PMCPMC8627925
OpenAlexW3184255150

What OpenQuestion holds

Textmetadata
LicenceTDM
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.