Evidence map›Paper›PMID 22098917›Full record

ArticleCancer cell international2011

Arsenic, cadmium and neuron specific enolase (ENO2, γ-enolase) expression in breast cancer.

Maureen A Soh, Scott H Garrett, Seema Somji, Jane R Dunlevy, Xu Dong Zhou, Mary Ann Sens, Chandra S Bathula, Christina Allen, Donald A Sens

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. BeyondMolecular therapy oncolytics · 2023
    Review
  7. Article
  8. Aerobic glycolysis in colon cancer is repressed by naringin via theJournal of Zhejiang University. Science. B · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Prognostic Value of Enolase Gene Family in Colon Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  15. Article
  16. Review
  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

9 authors at 1 institution in 1 country.

Maureen A SohDepartment of Pathology, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND, USA. donald.sens@med.und.edu.
Scott H Garrett
Seema Somji
Jane R Dunlevy
Xu Dong Zhou
Mary Ann Sens
Chandra S Bathula
Christina Allen
Donald A Sens
University of North Dakota · US

Funding

WORKSHOPS AND EVALUATIONP20RR016471 · NCRR · UNIVERSITY OF NORTH DAKOTA · PI DELORME, EUGENE L. · 2001 to 2011
$31.7M
Steering Undergraduate Interest in Environmental Health Sciences at the UniversitR25ES016250 · NIEHS · UNIVERSITY OF NORTH DAKOTA · PI SENS, DONALD A. · 2008 to 2012
$278k
NCRR NIH HHS P20 RR016471NIEHS NIH HHS R25 ES016250
6 · The paper itself

Abstract

backgroundNeuron specific enolase (ENO2, γ-enolase) has been used as a biomarker to help identify neuroendocrine differentiation in breast cancer. The goal of the present study was to determine if ENO2 expression in the breast epithelial cell is influenced by the environmental pollutants, arsenite and cadmium. Acute and chronic exposure of MCF-10A cells to As+3 and Cd+2 sufficient to allow colony formation in soft agar, was used to determine if ENO2 expression was altered by these pollutants.

resultsIt was shown that both As+3 and Cd+2 exposure caused significant increases in ENO2 expression under conditions of both acute and chronic exposure. In contrast, ENO1, the major glycolytic enolase in non-muscle and neuronal cells, was largely unaffected by exposure to either As+3 or Cd+2. Localization studies showed that ENO2 in the MCF-10A cells transformed by As+3 or Cd+2 had both a cytoplasmic and nuclear localization. In contrast, ENO1 was localized to the cytoplasm. ENO2 localized to the cytoplasm was found to co-localized with ENO1.

conclusionThe results are the first to show that ENO2 expression in breast epithelial cells is induced by acute and chronic exposure to As+3 or Cd+2. The findings also suggest a possible link between As+3 and Cd+2 exposure and neuroendocrine differentiation in tumors. Overall, the results suggest that ENO2 might be developed as a biomarker indicating acute and/or chronic environmental exposure of the breast epithelial cell to As+3 and Cd+2.

Identifiers

PMID22098917
PMCPMC3233504
OpenAlexW1996510149

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.