Exposure to 900 MHz electromagnetic field induces an unbalance between pro-apoptotic and pro-survival signals in T-lymphoblastoid leukemia CCRF-CEM cells.

Journal of cellular physiology · 2004 · Mixed · Low evidence

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MixedLow evidencePaper 5242

Study snapshot

PublicationJournal of cellular physiology · 2004

Study typein_vitro

Reported directionMixed

Evidence ratingLow

Abstract

It has been recently established that low-frequency electromagnetic field (EMFs) exposure induces biological changes and could be associated with increased incidence of cancer, while the issue remains unresolved as to whether high-frequency EMFs can have hazardous effect on health. Epidemiological studies on association between childhood cancers, particularly leukemia and brain cancer, and exposure to low- and high-frequency EMF suggested an etiological role of EMFs in inducing adverse health effects. To investigate whether exposure to high-frequency EMFs could affect in vitro cell survival, we cultured acute T-lymphoblastoid leukemia cells (CCRF-CEM) in the presence of unmodulated 900 MHz EMF, generated by a transverse electromagnetic (TEM) cell, at various exposure times. We evaluated the effects of high-frequency EMF on cell growth rate and apoptosis induction, by cell viability (MTT) test, FACS analysis and DNA ladder, and we investigated pro-apoptotic and pro-survival signaling pathways possibly involved as a function of exposure time by Western blot analysis. At short exposure times (2-12 h), unmodulated 900 MHz EMF induced DNA breaks and early activation of both p53-dependent and -independent apoptotic pathways while longer continuous exposure (24-48 h) determined silencing of pro-apoptotic signals and activation of genes involved in both intracellular (Bcl-2) and extracellular (Ras and Akt1) pro-survival signaling. Overall our results indicate that exposure to 900 MHz continuous wave, after inducing an early self-defense response triggered by DNA damage, could confer to the survivor CCRF-CEM cells a further advantage to survive and proliferate.

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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 directionmixed

PopulationAcute T-lymphoblastoid leukemia cells (CCRF-CEM)

Sample sizeNot supplied

ExposureRF · 900 MHz · 2–48 h (short: 2–12 h; long: 24–48 h)

Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

In CCRF-CEM cells exposed in vitro to unmodulated 900 MHz EMF, short exposures (2–12 h) induced DNA breaks and early activation of p53-dependent and p53-independent apoptotic pathways. Longer continuous exposure (24–48 h) was associated with silencing of pro-apoptotic signals and activation of pro-survival signaling (including Bcl-2, Ras, Akt1), which the authors interpret as conferring a survival/proliferation advantage to surviving cells.

Outcomes measured

Cell growth rate
Cell viability (MTT)
Apoptosis induction (FACS analysis, DNA ladder)
DNA breaks
p53-dependent apoptotic pathway activation
p53-independent apoptotic pathway activation
Pro-apoptotic signaling (silencing at longer exposure)
Pro-survival signaling (Bcl-2, Ras, Akt1 activation)

Limitations

In vitro cell-line study; findings may not translate to in vivo or human health outcomes
No dosimetry details reported in the abstract (e.g., SAR, field strength)
Sample size/replication not reported in the abstract

View raw extracted JSON

{
  "study_type": "in_vitro",
  "exposure": {
    "band": "RF",
    "source": null,
    "frequency_mhz": 900,
    "sar_wkg": null,
    "duration": "2–48 h (short: 2–12 h; long: 24–48 h)"
  },
  "population": "Acute T-lymphoblastoid leukemia cells (CCRF-CEM)",
  "sample_size": null,
  "outcomes": [
    "Cell growth rate",
    "Cell viability (MTT)",
    "Apoptosis induction (FACS analysis, DNA ladder)",
    "DNA breaks",
    "p53-dependent apoptotic pathway activation",
    "p53-independent apoptotic pathway activation",
    "Pro-apoptotic signaling (silencing at longer exposure)",
    "Pro-survival signaling (Bcl-2, Ras, Akt1 activation)"
  ],
  "main_findings": "In CCRF-CEM cells exposed in vitro to unmodulated 900 MHz EMF, short exposures (2–12 h) induced DNA breaks and early activation of p53-dependent and p53-independent apoptotic pathways. Longer continuous exposure (24–48 h) was associated with silencing of pro-apoptotic signals and activation of pro-survival signaling (including Bcl-2, Ras, Akt1), which the authors interpret as conferring a survival/proliferation advantage to surviving cells.",
  "effect_direction": "mixed",
  "limitations": [
    "In vitro cell-line study; findings may not translate to in vivo or human health outcomes",
    "No dosimetry details reported in the abstract (e.g., SAR, field strength)",
    "Sample size/replication not reported in the abstract"
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "900 MHz",
    "radiofrequency",
    "continuous wave",
    "unmodulated",
    "TEM cell",
    "CCRF-CEM",
    "T-lymphoblastoid leukemia",
    "apoptosis",
    "DNA damage",
    "p53",
    "Bcl-2",
    "Ras",
    "Akt1"
  ],
  "suggested_hubs": []
}

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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: 10.1002/jcp.10425
PubMed: 14603534

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