Evidence map›Paper›PMID 17384772›Full record

ArticleEnvironmental health perspectives2007

Mechanisms of acquired androgen independence during arsenic-induced malignant transformation of human prostate epithelial cells.

Lamia Benbrahim-Tallaa, Mukta M Webber, Michael P Waalkes

Open access · diamondAbstract read
In one paragraph

Article in Environmental health perspectives, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 pooled it
2.3field-weighted citation impact, top 12% 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, 2 syntheses or guidelines pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Arsenic-induced prostate cancer: an enigma.Medical oncology (Northwood, London, England) · 2024
    Review
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  16. Article
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  18. Endocrine disruptors and prostate cancer risk.Endocrine-related cancer · 2008
    Review
  19. Article
  20. Inorganic arsenic and human prostate cancer.Environmental health perspectives · 2008
    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

3 authors at 2 institutions in 1 country.

Lamia Benbrahim-TallaaLaboratory of Comparative Carcinogenesis, National Cancer Institute at the National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina 27709, USA.
Mukta M Webber
Michael P Waalkes
National Institutes of Health · USMichigan State University · US

Funding

MECHANISMS OF INORGANIC CARCINOGENESISZ01BC005488 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WAALKES, MICHAEL · 1996 to 2008
$3.4M
Mechanisms of Inorganic CarcinogenesisZIABC005488 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WAALKES, MICHAEL · 2009 to 2010
$2.5M
6 · The paper itself

Abstract

backgroundProstate cancer progression often occurs with overexpression of growth factors and receptors, many of which engage the Ras/mitogen-activated protein MAP kinase (MAPK) pathway.

objectivesIn this study we used arsenic-transformed human prostate epithelial cells, which also show androgen-independent growth, to study the possibility that chronic activation of Ras/MAPK signaling may contribute to arsenic-induced prostate cancer progression.

methodsControl and chronic arsenic-transformed prostate epithelial cells (CAsE-PE) were compared for Ras/MAPK signaling capacities using reverse transcription-polymerase chain reaction and Western blot analyses.

resultsWe found activation of HER-2/neu oncogene in transformed CAsE-PE cells, providing molecular evidence of androgen independence in the transformed cells. CAsE-PE cells displayed constitutively increased expression of unmutated K-Ras (6-fold), and the downstream MAP kinases A-Raf and B-Raf (2.2-fold and 3.2-fold, respectively). There was also increased expression of phosphorylated MEK1/2 and Elk1 in the transformant cells. The MEK1/2 inhibitor, U0126, blocked PSA overexpression in CAsE-PE cells.

conclusionThus, arsenic-induced malignant transformation and acquired androgen independence are linked to Ras signaling activation in human prostate epithelial cells. Chronic activation of this pathway can sensitize the androgen receptor to subphysiologic levels of androgen. This may be important in arsenic carcinogenesis and provide a mechanism that may be common for prostate cancer progression driven by diverse agents.

Indexed as

AndrogensArsenicBlotting, WesternCell ProliferationCells, CulturedCell Transformation, NeoplasticEnvironmental PollutantsEpithelial CellsErb-b2 Receptor Tyrosine KinasesHumansMaleMAP Kinase Signaling SystemModels, BiologicalProstateProstatic NeoplasmsProto-Oncogene Proteins p21(ras)AndrogensAR protein, humanArsenicEnvironmental PollutantsErb-b2 Receptor Tyrosine KinasesProto-Oncogene Proteins p21(ras)raf KinasesReceptors, Androgen

Identifiers

PMID17384772
PMCPMC1817693
OpenAlexW2061939832

What OpenQuestion holds

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Registered trials

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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.