Evidence map›Paper›PMID 22331493›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2012

Sodium arsenite ± hyperthermia sensitizes p53-expressing human ovarian cancer cells to cisplatin by modulating platinum-DNA damage responses.

Clarisse S Muenyi, Allan R Pinhas, Teresa W Fan, Guy N Brock, C William Helm, J Christopher States

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Arsenoplatin-1 Is a Dual Pharmacophore Anticancer Agent.Journal of the American Chemical Society · 2019
    Article
  8. Applications of Focused Ultrasound in Cerebrovascular Diseases and Brain Tumors.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Disruption of Mitotic Progression by Arsenic.Biological trace element research · 2015
    Review
  14. 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

6 authors at 3 institutions in 1 country.

Clarisse S MuenyiDepartment of Pharmacology and Toxicology, University of Louisville, Louisville, Kentucky 40292, USA.
Allan R Pinhas
Teresa W Fan
Guy N Brock
C William Helm
J Christopher States
University of Louisville · USDivision of Chemistry · USSaint Louis University · US

Funding

Strategic Vision & Impact on Environmental HealthP30ES014443 · NIEHS · UNIVERSITY OF LOUISVILLE · PI PROUGH, RUSSELL ALLEN · 2007 to 2010
$4.4M
Arsenic Induced Miotic Arrest Associated ApoptosisR01ES011314 · NIEHS · UNIVERSITY OF LOUISVILLE · PI STATES, J CHRISTOPHER · 2003 to 2009
$1.4M
NIEHS NIH HHS P30 ES014443NIEHS NIH HHS R01 ES011314
6 · The paper itself

Abstract

Epithelial ovarian cancer (EOC) is the leading cause of gynecological cancer death in the United States. Cisplatin is a DNA damaging agent initially effective against EOC but limited by resistance. P53 plays a critical role in cellular response to DNA damage and has been implicated in EOC response to platinum chemotherapy. In this study, we examined the role of p53 status in EOC response to a novel combination of cisplatin, sodium arsenite, and hyperthermia. Human EOC cells were treated with cisplatin ± 20μM sodium arsenite at 37°C or 39°C for 1 h. Sodium arsenite ± hyperthermia sensitized wild-type p53-expressing (A2780, A2780/CP70, OVCA 420, OVCA 429, and OVCA 433) EOC cells to cisplatin. Hyperthermia sensitized p53-null SKOV-3 and p53-mutant (OVCA 432 and OVCAR-3) cells to cisplatin. P53 small interfering RNA (siRNA) transfection abrogated sodium arsenite sensitization effect. XPC, a critical DNA damage recognition protein in global genome repair pathway, was induced by cisplatin only in wild-type p53-expressing cells. Cotreatment with sodium arsenite ± hyperthermia attenuated cisplatin-induced XPC in wild-type p53-expressing cells. XPC siRNA transfection sensitized wild-type p53-expressing cells to cisplatin, suggesting that sodium arsenite ± hyperthermia attenuation of XPC is a mechanism by which wild-type p53-expressing cells are sensitized to cisplatin. Hyperthermia ± sodium arsenite enhanced cellular and DNA accumulation of platinum in wild-type p53-expressing cells. Only hyperthermia enhanced platinum accumulation in p53-null cells. In conclusion, sodium arsenite ± hyperthermia sensitizes wild-type p53-expressing EOC cells to cisplatin by suppressing DNA repair protein XPC and increasing cellular and DNA platinum accumulation.

Indexed as

Hyperthermia, InducedAntineoplastic AgentsArsenitesCell Line, TumorCell SurvivalCisplatinDNA-Binding ProteinsDNA DamageDrug Resistance, NeoplasmDrug Screening Assays, AntitumorDrug Therapy, CombinationFemaleHumansOvarian NeoplasmsRNA, Small InterferingSodium CompoundsAntineoplastic AgentsArsenitesCisplatinDNA-Binding ProteinsRNA, Small Interferingsodium arseniteSodium CompoundsTumor Suppressor Protein p53XPC protein, human

Identifiers

PMID22331493
PMCPMC3327868
OpenAlexW2098460586

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.