Evidence map›Paper›PMID 20045430›Full record

ArticleToxicology and applied pharmacology2010

Low level exposure to monomethyl arsonous acid-induced the over-production of inflammation-related cytokines and the activation of cell signals associated with tumor progression in a urothelial cell model.

C Escudero-Lourdes, M K Medeiros, M C Cárdenas-González, S M Wnek, J A Gandolfi

Abstract readComparative Study
In one paragraph

Article in Toxicology and applied pharmacology, 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
5.4field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Arsenic Exposure and Compromised Protein Quality Control.Chemical research in toxicology · 2020
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Arsenic and Chronic Kidney Disease: A Systematic Review.Current environmental health reports · 2014
    Article
  12. Article
  13. Urine arsenic and prevalent albuminuria: evidence from a population-based study.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2013
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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 2 institutions in 2 countries.

C Escudero-LourdesFacultad de Ciencias Químicas, Universidad Autónoma de San Luis Potosí, San Luis Potosí, SLP 78240, Mexico. cescuder@uaslp.mx
M K Medeiros
M C Cárdenas-González
S M Wnek
J A Gandolfi
University of Arizona · USAutonomous University of San Luis Potosí · MX

Funding

TRANSPORT OF TRACE METALS IN A POLLUTED AQUIFERP42ES004940 · NIEHS · UNIVERSITY OF ARIZONA · PI Xinxin Ding · 1990 to 2026
$68.1M
SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI DEAN BILLHEIMER · 1994 to 2026
$36.7M
NIEHS NIH HHS ES 04940NIEHS NIH HHS ES 06694NIEHS NIH HHS P30 ES006694NIEHS NIH HHS P42 ES004940
6 · The paper itself

Abstract

Human bladder cancer has been associated with chronic exposure to arsenic. Chronic exposure of an immortalized non-tumorigenic urothelial cell line (UROtsa cells) to arsenicals has transformed these cells to a malignant phenotype, but the involved mechanisms are not fully understood. Chronic inflammation has been linked with cancer development mainly because many pro-inflammatory cytokines, growth factors as well as angiogenic chemokines have been found in tumors. In this study the chronology of inflammatory cytokines production was profiled in UROtsa cells chronically exposed to the toxic arsenic metabolite, monomethylarsonous acid [50 nM MMA(III)] to know the role of inflammation in cell transformation. Acute 50 nM MMA(III) exposure induced over-production of many pro-inflammatory cytokines as soon as 12 h after acute exposure. The same cytokines remain over-regulated after chronic exposure to 50 nM MMA(III), especially after 3 mo exposure. At 3 mo exposure the sustained production of cytokines like IL-1, IL-6, IL-8 and TNF is coincident with the appearance of characteristics associated with cell transformation seen in other arsenic-UROtsa studies. The sustained and increased activation of NFkappaB and c-Jun is also present along the transformation process and the phosphorylated proteins p38 MAPK and ERK 1/2 are increased also through the time line. Taken together these results support the notion that chronic inflammation is associated within MMA(III)-induced cell transformation and may act as a promoting factor in UROtsa cell transformation.

Indexed as

Cell Line, TransformedCell Transformation, NeoplasticCytokinesHumansInflammation MediatorsOrganometallic CompoundsSignal TransductionUrinary Bladder NeoplasmsUrotheliumCytokinesInflammation Mediatorsmonomethylarsonous acidOrganometallic Compounds

Identifiers

PMID20045430
PMCPMC2846965
OpenAlexW1987285533

What OpenQuestion holds

Textmetadata
LicenceTDM
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.