DNMT1 and miRNAs: possible epigenetics footprints in electromagnetic fields utilization in oncology

Medical oncology (Northwood, London, England) · 2021 · Mixed · Insufficient evidence

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MixedInsufficient evidencePaper 1044

This review summarizes reports suggesting ELF-EMF exposures can alter epigenetic machinery directly or via signaling pathways, with potential implications for cancer cell homeostasis and processes such as DNA repair, apoptosis, metastasis, differentiation, an…

Study snapshot

PublicationMedical oncology (Northwood, London, England) · 2021
Study typereview
Reported directionMixed
Evidence ratingInsufficient

Abstract

DNMT1 and miRNAs: possible epigenetics footprints in electromagnetic fields utilization in oncology Mohadeseh Shayeghan, Flora Forouzesh, Alireza Madjid Ansari, Mohammad Amin Javidi. DNMT1 and miRNAs: possible epigenetics footprints in electromagnetic fields utilization in oncology. Med Oncol. 2021 Sep 8;38(10):125. doi: 10.1007/s12032-021-01574-y. Abstract Many studies were performed to unravel the effects of different types of Electromagnetic fields (EMFs) on biological systems. Some studies were conducted to exploit EMFs for medical purposes mainly in cancer therapy. Although many studies suggest that the EMFs exposures can be effective in pre-clinical cancer issues, the treatment outcomes of these exposures on the cancer cells, especially at the molecular level, are challenging and overwhelmingly complicated yet. This article aims to review the epigenetic mechanisms that can be altered by EMFs exposures with the main emphasis on Extremely low frequency electromagnetic field (ELF-EMF). The epigenetic mechanisms are reversible and affected by environmental factors, thus, EMFs exposures can modulate these mechanisms. According to the reports, ELF-EMF exposures affect epigenetic machinery directly or through the molecular signaling pathways. ELF-EMF in association with DNA methylation, histone modification, miRNAs, and nucleosome remodeling could affect the homeostasis of cancer cells and play a role in DNA damage repairing, apoptosis induction, prevention of metastasis, differentiation, and cell cycle regulation. In general, the result of this study shows that ELF-EMF exposure probably can be effective in cancer epigenetic therapy, but more molecular and clinical investigations are needed to clarify the safe and specific dosimetric characteristics of ELF-EMF in practice. pubmed.ncbi.nlm.nih.gov

Machine Enhanced Logic

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 typereview
Effect directionmixed
PopulationNot supplied
Sample sizeNot supplied
ExposureELF
Evidence strengthInsufficientConfidence: 74% · Peer reviewed: yes

Main findings

This review summarizes reports suggesting ELF-EMF exposures can alter epigenetic machinery directly or via signaling pathways, with potential implications for cancer cell homeostasis and processes such as DNA repair, apoptosis, metastasis, differentiation, and cell cycle regulation. The authors conclude ELF-EMF exposure probably can be effective in cancer epigenetic therapy, but more molecular and clinical studies are needed to clarify safe and specific dosimetric characteristics.

Outcomes measured

  • Epigenetic mechanisms (DNA methylation, histone modification, miRNAs, nucleosome remodeling)
  • Cancer cell homeostasis
  • DNA damage repair
  • Apoptosis
  • Metastasis prevention
  • Differentiation
  • Cell cycle regulation

Limitations

  • Review article; no primary data presented in abstract
  • Treatment outcomes described as challenging and complicated at the molecular level
  • Authors note need for additional molecular and clinical investigations
  • Safe and specific dosimetric characteristics not yet clarified
View raw extracted JSON
{
  "study_type": "review",
  "exposure": {
    "band": "ELF",
    "source": "medical/oncology therapy (EMF utilization)",
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": null
  },
  "population": null,
  "sample_size": null,
  "outcomes": [
    "Epigenetic mechanisms (DNA methylation, histone modification, miRNAs, nucleosome remodeling)",
    "Cancer cell homeostasis",
    "DNA damage repair",
    "Apoptosis",
    "Metastasis prevention",
    "Differentiation",
    "Cell cycle regulation"
  ],
  "main_findings": "This review summarizes reports suggesting ELF-EMF exposures can alter epigenetic machinery directly or via signaling pathways, with potential implications for cancer cell homeostasis and processes such as DNA repair, apoptosis, metastasis, differentiation, and cell cycle regulation. The authors conclude ELF-EMF exposure probably can be effective in cancer epigenetic therapy, but more molecular and clinical studies are needed to clarify safe and specific dosimetric characteristics.",
  "effect_direction": "mixed",
  "limitations": [
    "Review article; no primary data presented in abstract",
    "Treatment outcomes described as challenging and complicated at the molecular level",
    "Authors note need for additional molecular and clinical investigations",
    "Safe and specific dosimetric characteristics not yet clarified"
  ],
  "evidence_strength": "insufficient",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "ELF-EMF",
    "electromagnetic fields",
    "oncology",
    "cancer therapy",
    "epigenetics",
    "DNMT1",
    "DNA methylation",
    "histone modification",
    "miRNAs",
    "nucleosome remodeling",
    "apoptosis",
    "metastasis",
    "cell cycle",
    "DNA repair"
  ],
  "suggested_hubs": [
    {
      "slug": "oncology-therapeutic-emf",
      "weight": 0.78,
      "reason": "Focuses on exploiting EMFs (especially ELF-EMF) for cancer therapy and epigenetic mechanisms."
    }
  ]
}
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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: 10.1007/s12032-021-01574-y
PubMed: 34495398

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