Evidence map›Paper›PMID 27449664›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2016

Prolonged Particulate Hexavalent Chromium Exposure Suppresses Homologous Recombination Repair in Human Lung Cells.

Cynthia L Browning, Qin Qin, Deborah F Kelly, Rohit Prakash, Fabio Vanoli, Maria Jasin, John Pierce Wise

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. It's a gator tale: Alligator lung cells resist hexavalent chromium-induced DNA repair inhibition and chromosome instability.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2026
    Article
  4. 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
  5. Hexavalent chromium exposure impacts the metabolome of human lung fibroblast cells.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2025
    Article
  6. Oropharyngeal aspiration of particulate hexavalent chromium increases chromium levels in lung and liver, and induces essential metal dyshomeostasis in lung, liver, and blood.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2025
    Article
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  10. Review
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  13. A whale of a tale: whale cells evade the driving mechanism for hexavalent chromium-induced chromosome instability.Toxicological sciences : an official journal of the Society of Toxicology · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Particulate Hexavalent Chromium Inhibits E2F1 Leading to Reduced RAD51 Nuclear Foci Formation in Human Lung Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2021
    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

7 authors at 4 institutions in 1 country.

Cynthia L Browning*Wise Laboratory of Environmental and Genetic Toxicology, Portland, Maine 04104 Graduate School of Biomedical Science and Engineering, University of Maine, Orono, Maine 04469.
Qin Qin*Wise Laboratory of Environmental and Genetic Toxicology, Portland, Maine 04104 Virginia Tech Carilion Research Institute, Roanoke, Virginia 24016.
Deborah F KellyVirginia Tech Carilion Research Institute, Roanoke, Virginia 24016.
Rohit PrakashMemorial Sloan Kettering Cancer Center, New York 10065, New York.
Fabio VanoliMemorial Sloan Kettering Cancer Center, New York 10065, New York.
Maria JasinMemorial Sloan Kettering Cancer Center, New York 10065, New York.
John Pierce Wise*Wise Laboratory of Environmental and Genetic Toxicology, Portland, Maine 04104 Graduate School of Biomedical Science and Engineering, University of Maine, Orono, Maine 04469 john.wise@louisville.edu.
Memorial Sloan Kettering Cancer Center · USSociety of Environmental Toxicology and Chemistry · USUniversity of Maine · USVirginia Tech · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
RADIATION RESISTANT AND SENSITIVE CELLS DNA BREAK REPAIRR01GM054668 · NIGMS · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI JASIN, MARIA · 1998 to 2015
$5.3M
PARTICULATE CR(VI) TOXICOLOGY IN HUMAN LUNG EPITHELIAL CELLS AND FIBROBLASTS (Admin Supplement/PA-17-055)R01ES016893 · NIEHS · UNIVERSITY OF SOUTHERN MAINE · PI WISE, JOHN PIERCE · 2009 to 2021
$5.1M
NCI NIH HHS P30 CA008748NIEHS NIH HHS R01 ES016893NIGMS NIH HHS R01 GM054668
6 · The paper itself

Abstract

Genomic instability is one of the primary models of carcinogenesis and a feature of almost all cancers. Homologous recombination (HR) repair protects against genomic instability by maintaining high genomic fidelity during the repair of DNA double strand breaks. The defining step of HR repair is the formation of the Rad51 nucleofilament, which facilitates the search for a homologous sequence and invasion of the template DNA strand. Particulate hexavalent chromium (Cr(VI)), a human lung carcinogen, induces DNA double strand breaks and chromosome instability. Since the loss of HR repair increases Cr(VI)-induced chromosome instability, we investigated the effect of extended Cr(VI) exposure on HR repair. We show acute (24 h) Cr(VI) exposure induces a normal HR repair response. In contrast, prolonged (120 h) exposure to particulate Cr(VI) inhibited HR repair and Rad51 nucleofilament formation. Prolonged Cr(VI) exposure had a profound effect on Rad51, evidenced by reduced protein levels and Rad51 mislocalization to the cytoplasm. The response of proteins involved in Rad51 nuclear import and nucleofilament formation displayed varying responses to prolonged Cr(VI) exposure. BRCA2 formed nuclear foci after prolonged Cr(VI) exposure, while Rad51C foci formation was suppressed. These results suggest that particulate Cr(VI), a major chemical carcinogen, inhibits HR repair by targeting Rad51, causing DNA double strand breaks to be repaired by a low fidelity, Rad51-independent repair pathway. These results further enhance our understanding of the underlying mechanism of Cr(VI)-induced chromosome instability and thus, carcinogenesis.

Indexed as

Cell Line, TransformedChromiumDNA RepairGenomic InstabilityHomologous RecombinationHumansLungRad51 RecombinaseChromiumchromium hexavalent ionRAD51 protein, humanRad51 Recombinasechromosome instabilityhomologous recombination repairparticulate chromium (VI)Rad51 nucleofilament

Identifiers

PMID27449664
PMCPMC5601504
OpenAlexW2483600409

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.