Evidence map›Paper›PMID 20937726›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2011

Carcinogenic effects of "whole-life" exposure to inorganic arsenic in CD1 mice.

Erik J Tokar, Bhalchandra A Diwan, Jerrold M Ward, Don A Delker, Michael P Waalkes

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
9.0field-weighted citation impact, top 1% 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

55 citing papers in PubMed, 126 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Arsenic-induced prostate cancer: an enigma.Medical oncology (Northwood, London, England) · 2024
    Review
  6. Update of the risk assessment of inorganic arsenic in food.EFSA journal. European Food Safety Authority · 2024
    Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Chronic and acute arsenic exposure enhance EGFR expression via distinct molecular mechanisms.Toxicology in vitro : an international journal published in association with BIBRA · 2020
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Prostate Cancer Incidence in U.S. Counties and Low Levels of Arsenic in Drinking Water.International journal of environmental research and public health · 2020
    Article
  17. Article
  18. Review
  19. Article
  20. Review
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 at 4 institutions in 1 country.

Erik J TokarLaboratory of Comparative Carcinogenesis, National Cancer Institute, National Institute of Environmental Health Sciences, The National Institute of Environmental Health Sciences, Research Triangle Park, Raleigh, North Carolina 27709, USA.
Bhalchandra A Diwan
Jerrold M Ward
Don A Delker
Michael P Waalkes
Global VetPathology · USNational Institutes of Health · USScience Applications International Corporation (United States) · USUniversity of Utah · US

Funding

Stem Cell ToxicologyZIAES102925 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI TOKAR, ERIK · 2010 to 2021
$25.3M
Intramural NIH HHS
6 · The paper itself

Abstract

In a previously developed mouse model, arsenic exposure in utero induces tumors at multiple sites in the offspring as adults, often duplicating human targets. However, human environmental inorganic arsenic exposure occurs during the entire life span, not just part of gestation. Thus, "whole-life" inorganic arsenic carcinogenesis in mice was studied. CD1 mice were exposed to 0, 6, 12, or 24 ppm arsenic in the drinking water 2 weeks prior to breeding, during pregnancy, lactation, and after weaning through adulthood. Tumors were assessed in offspring until 2 years of age. Arsenic induced dose-related increases in lung adenocarcinoma (both sexes), hepatocellular carcinoma (both sexes), gallbladder tumors (males), and uterine carcinomas. Arsenic induced dose-related increases in ovarian tumors (including carcinomas) starting with the lowest dose. Adrenal tumors increased at all doses (both sexes). Arsenic-induced lung and liver cancers were highly enriched for cancer stem cells, consistent with prior work with skin cancers stimulated by prenatal arsenic. Reproductive tract tumors overexpressed cyclooxygenase-2 and estrogen receptor-α. Arsenic target sites were remarkably similar to prior transplacental studies, although tumors from whole-life exposure were generally more aggressive and frequent. This may indicate that arsenic-induced events in utero dictate target site in some tissues, whereas other exposure periods of arsenic enhance incidence or progression, though other factors could be at play, like cumulative dose. Whole-life arsenic exposure induced tumors at dramatically lower external doses than in utero arsenic only while more realistically duplicating human exposure.

Indexed as

AnimalsArsenitesCarcinogenicity TestsCarcinogens, EnvironmentalCell ProliferationDose-Response Relationship, DrugFemaleMaleMaternal ExposureMiceMice, Inbred StrainsNeoplasms, ExperimentalOrgan SpecificityPregnancySodium CompoundsTime FactorsArsenitesCarcinogens, Environmentalsodium arseniteSodium Compounds

Identifiers

PMID20937726
PMCPMC3003832
OpenAlexW2110467298

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.