Evidence map›Paper›PMID 12162446›Full record

ReviewMolecular and cellular biochemistry

Molecular mechanisms of Cr(VI)-induced carcinogenesis.

Min Ding, Xianglin Shi

Abstract readReview
PubMed
In one paragraph

Review in Molecular and cellular biochemistry. 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
–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

28 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. The dual roles of c-Jun NH2-terminal kinase signaling in Cr(VI)-induced apoptosis in JB6 cells.Toxicological sciences : an official journal of the Society of Toxicology · 2011
    Article
  16. Article
  17. Chromium genotoxicity: A double-edged sword.Chemico-biological interactions · 2010
    Review
  18. Article
  19. Article
  20. 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

2 authors.

Min DingPathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USA.
Xianglin Shi

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although Cr(VI)-containing compounds are well documented carcinogens, their mechanism of action is still not well understood. Recent studies have suggested that reduction of Cr(VI) to its lower oxidation states and related free radical reactions play an important role in Cr(VI)-induced carcinogenesis. This article summarizes recent studies from our laboratory on (a) the reduction of Cr(VI) by ascorbate, diol- and thiol-containing molecules, certain flavoenzymes, cell organelles, intact cells, and whole animals; (b) free radical production in both non-cellular and cellular systems; and (c) Cr(VI)-induced DNA damage, activation of nuclear transcription factor KB (NF-kappaB), activator protein-1, p53, hypoxia-inducible factor-1, vascular endothelial growth factor, tyrosine phosphorylation, apoptosis, cell growth arrest, and gene expression profile.

Indexed as

AnimalsCarcinogensCell CycleCell Transformation, NeoplasticChromiumDNA DamageFree RadicalsGene Expression Regulation, NeoplasticHumansOxidation-ReductionCarcinogensChromiumchromium hexavalent ionFree Radicals

Identifiers

PMID12162446

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.