Effects of 60-Hz fields, estradiol and xenoestrogens on human breast cancer cells.

Radiation research · 1996 · No effect · Low evidence

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No effectLow evidencePaper 5429

Estradiol and xenoestrogens (DDT and Red No. 3) increased Cdk2 and cyclin B1-cdc2 activity and cyclin D1 synthesis, and stimulated estrogen receptor binding to the estrogen response element. Exposure to 60-Hz electromagnetic fields at 12 mG or 1 or 9 G did no…

Study snapshot

PublicationRadiation research · 1996
Study typein_vitro
Reported directionNo effect
Evidence ratingLow

Abstract

If exposure to xenoestrogens or electromagnetic fields (EMFs) such as 60 Hz contributes to the etiology of breast cancer, it is likely that they must stimulate the growth of breast cells, damage genetic material or enhance the effects of other mitogenic or mutagenic agents (co-promotion). Therefore, the ability of xenoestrogens or exposure to 60-Hz fields to stimulate the entry of growth-arrested human breast cancer cells into the cell cycle was determined using cyclin-dependent kinase 2 (Cdk2) activity, synthesis of cyclin D1 and cdc2 activity. Exposure of estrogen receptor-positive MCF-7 or T-47D cells to estrogen and xenoestrogens (DDT and Red No. 3) increased Cdk2 and cyclin B1-cdc2 activity and cyclin D1 synthesis. Exposure of breast cancer cells to 12 mG or 1 or 9 G electromagnetic fields at 60 Hz failed to stimulate Cdk2 or cyclin B1-cdc2 activity or cyclin D1 synthesis. Simultaneous co-exposure of cells to 60-Hz fields and chemical promoters did not enhance Cdk2 activation above the levels produced by the chemical promoter alone. Estrogen and xenoestrogens also stimulated binding of the estrogen receptor to the estrogen receptor element but the EMF did not. Phorbol 12-myristate 13-acetate (PMA) induced phosphorylation of p53 and pRb1O5 in MCF-7 cells, but EMF exposure had no effect. DNA-damaging chemotherapeutic agents and Red Dye No. 3 were found to increase p53 site-specific DNA binding in breast cancer cells, but EMF exposure did not. Differential display analysis failed to detect any effect of EMF exposure on gene expression in MCF-7 cells, whereas the effects of estradiol were detected. These studies suggest that estrogen and xenoestrogens stimulate growth-arrested breast cancer cells to enter the growth cycle, but EMF exposure does not. Site-specific p53-DNA binding was increased in MC F-7 cells treated with DNA-damaging agents, but not by EMF exposure. EMF exposure does not appear to act as a promoter or DNA-damaging agent for human breast cancer cells in vitro.

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AI evidence extraction

Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.

Study typein_vitro
Effect directionno_effect
PopulationHuman breast cancer cell lines (MCF-7, T-47D; estrogen receptor-positive)
Sample sizeNot supplied
ExposureELF · 0.06 MHz
Evidence strengthLowConfidence: 86% · Peer reviewed: yes

Main findings

Estradiol and xenoestrogens (DDT and Red No. 3) increased Cdk2 and cyclin B1-cdc2 activity and cyclin D1 synthesis, and stimulated estrogen receptor binding to the estrogen response element. Exposure to 60-Hz electromagnetic fields at 12 mG or 1 or 9 G did not stimulate these cell-cycle markers, did not enhance effects of chemical promoters during co-exposure, and showed no effect on p53/pRb phosphorylation, p53 DNA binding, or gene expression in MCF-7 cells.

Outcomes measured

  • Cdk2 activity
  • Cyclin B1-cdc2 activity
  • Cyclin D1 synthesis
  • Estrogen receptor binding to estrogen response element
  • Phosphorylation of p53
  • Phosphorylation of pRb105
  • p53 site-specific DNA binding
  • Gene expression (differential display)

Limitations

  • In vitro study in breast cancer cell lines; may not generalize to in vivo breast tissue or cancer etiology
  • Exposure duration not reported in the abstract
  • Sample sizes/replicates not reported in the abstract
View raw extracted JSON
{
  "study_type": "in_vitro",
  "exposure": {
    "band": "ELF",
    "source": null,
    "frequency_mhz": 0.06,
    "sar_wkg": null,
    "duration": null
  },
  "population": "Human breast cancer cell lines (MCF-7, T-47D; estrogen receptor-positive)",
  "sample_size": null,
  "outcomes": [
    "Cdk2 activity",
    "Cyclin B1-cdc2 activity",
    "Cyclin D1 synthesis",
    "Estrogen receptor binding to estrogen response element",
    "Phosphorylation of p53",
    "Phosphorylation of pRb105",
    "p53 site-specific DNA binding",
    "Gene expression (differential display)"
  ],
  "main_findings": "Estradiol and xenoestrogens (DDT and Red No. 3) increased Cdk2 and cyclin B1-cdc2 activity and cyclin D1 synthesis, and stimulated estrogen receptor binding to the estrogen response element. Exposure to 60-Hz electromagnetic fields at 12 mG or 1 or 9 G did not stimulate these cell-cycle markers, did not enhance effects of chemical promoters during co-exposure, and showed no effect on p53/pRb phosphorylation, p53 DNA binding, or gene expression in MCF-7 cells.",
  "effect_direction": "no_effect",
  "limitations": [
    "In vitro study in breast cancer cell lines; may not generalize to in vivo breast tissue or cancer etiology",
    "Exposure duration not reported in the abstract",
    "Sample sizes/replicates not reported in the abstract"
  ],
  "evidence_strength": "low",
  "confidence": 0.86,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "60 Hz",
    "ELF magnetic fields",
    "MCF-7",
    "T-47D",
    "breast cancer cells",
    "estradiol",
    "xenoestrogens",
    "DDT",
    "Red No. 3",
    "cell cycle",
    "Cdk2",
    "cyclin D1",
    "cdc2",
    "p53",
    "gene expression"
  ],
  "suggested_hubs": [
    {
      "slug": "elf-emf",
      "weight": 0.9,
      "reason": "Study tests 60-Hz (ELF) magnetic field exposure effects in vitro."
    }
  ]
}
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AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.

Identifiers and source

DOI: Not supplied
PubMed: 8927716

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