Evidence map›Paper›PMID 20632473›Full record

ArticleInternational journal of environmental research and public health2010

Arsenic trioxide modulates DNA synthesis and apoptosis in lung carcinoma cells.

Alice M Walker, Jacqueline J Stevens, Kenneth Ndebele, Paul B Tchounwou

Abstract read
In one paragraph

Article in International journal of environmental research and public health, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. A candidate for lung cancer treatment: arsenic trioxide.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2019
    Review
  3. Review
  4. Endophytic Fungus Isolated FromFrontiers in oncology · 2018
    Article
  5. Article
  6. Molecular insight of arsenic-induced carcinogenesis and its prevention.Naunyn-Schmiedeberg's archives of pharmacology · 2017
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Enhancement of arsenic trioxide-mediated changes in human induced pluripotent stem cells (IPS).International journal of environmental research and public health · 2014
    Article
  13. Article
  14. Arsenic is cytotoxic and genotoxic to primary human lung cells.Mutation research. Genetic toxicology and environmental mutagenesis · 2014
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Heavy metal toxicity and the environment.Experientia supplementum (2012)
    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

4 authors.

Alice M WalkerMolecular Toxicology Research Laboratory, NIH RCMI-Center for Environmental Health, College of Science, Engineering and Technology, Jackson State University, Jackson, MS 39217, USA. alice.m.walker@jsums.edu
Jacqueline J Stevens
Kenneth Ndebele
Paul B Tchounwou

Funding

TRANSCRIPTOMICS OF GIARDIA LAMBLIAG12RR013459 · NCRR · JACKSON STATE UNIVERSITY · PI TCHOUNWOU, PAUL B. · 1998 to 2011
$18.0M
NCRR NIH HHS 5G12RR013459-12NCRR NIH HHS G12 RR013459
6 · The paper itself

Abstract

Arsenic trioxide, the trade name Trisenox, is a drug used to treat acute promyleocytic leukemia (APL). Studies have demonstrated that arsenic trioxide slows cancer cells growth. Although arsenic influences numerous signal-transduction pathways, cell-cycle progression, and/or apoptosis, its apoptotic mechanisms are complex and not entirely delineated. The primary objective of this research was to evaluate the effects of arsenic trioxide on DNA synthesis and to determine whether arsenic-induced apoptosis is mediated via caspase activation, p38 mitogen-activated protein kinase (MAPK), and cell cycle arrest. To achieve this goal, lung cancer cells (A549) were exposed to various concentrations (0, 2, 4, 6, 8, and 10 microg/mL) of arsenic trioxide for 48 h. The effect of arsenic trioxide on DNA synthesis was determined by the [3H]thymidine incorporation assay. Apoptosis was determined by the caspase-3 fluorescein isothiocyanate (FITC) assay, p38 MAP kinase activity was determined by an immunoblot assay, and cell-cycle analysis was evaluated by the propidium iodide assay. The [3H]thymidine-incorporation assay revealed a dose-related cytotoxic response at high levels of exposure. Furthermore, arsenic trioxide modulated caspase 3 activity and induced p38 MAP kinase activation in A549 cells. However, cell-cycle studies showed no statistically significant differences in DNA content at subG1 check point between control and arsenic trioxide treated cells.

Indexed as

ApoptosisArsenicalsArsenic TrioxideCaspase 3Cell CycleCell Line, TumorDNA ReplicationHumansLung NeoplasmsOxidesp38 Mitogen-Activated Protein KinasesThymidineArsenicalsArsenic TrioxideCaspase 3Oxidesp38 Mitogen-Activated Protein KinasesThymidine

Identifiers

PMID20632473
PMCPMC2864039

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.