Study type: Medical/biological study (experimental study)

Cancer cell proliferation is inhibited by specific modulation frequencies med./bio.

Published in: Br J Cancer 2012; 106 (2): 307-313

Aim of study (acc. to editor)

To study the effects of amplitude modulated electromagnetic fields on the cell proliferation of cancer cells. The authors aimed to investigate the mechanism of action of amplitude modulated electromagnetic fields used in previous clinical studies for the treatment of cancer patients (Barbault et la. 2009 and Costa et la. 2011).

Background/further details

There is clinical evidence that very low levels of amplitude modulated electromagnetic fields administered via an intrabuccal spoon-shaped probe may elicit therapeutic responses in patients with cancer. To understand the mechanism of this approach, hepatocellular carcinoma cells were exposed to 27.12 MHz radiofrequency electromagnetic fields to replicate the in vivo conditions. Additionally, cancer cells were exposed to tumour-specific modulation frequencies, previously identified by "biofeedback" methods in patients with a diagnosis of cancer (Barbault et la. 2009). Using such a patient-based "biofeedback" approach, Barbault et la. 2009 identified strikingly similar frequencies among patients with the same type of cancer and observed that patients with a different type of cancer had "biofeedback" responses to different frequencies.
Control modulation frequencies consisted of randomly chosen modulation frequencies.
Two different in vitro exposure systems were used to expose cells in culture (parallel plate capacitor and TEM cell).

Endpoint

Exposure

Exposure Parameters
Exposure 1: 27.12 MHz
Modulation type: AM
Exposure duration: continuous for 1 h/day, 3 h/day or 6 h/day for 7 days or 3 h/day for 3 days
  • SAR: 0.03 W/kg (average at the monolayer)
  • SAR: 0.05 W/kg (for additional experiments)
  • SAR: 0.1 W/kg (for additional experiments)
  • SAR: 1 W/kg (for additional experiments)
Exposure 2: 27.12 MHz
Modulation type: AM
Exposure duration: continuous for 1 h/day, 3 h/day or 6 h/day for 7 days or 3 h/day for 3 days
  • SAR: 0.03 W/kg (average at the monolayer)
  • SAR: 0.05 W/kg (for additional experiments)
  • SAR: 0.1 W/kg (for additional experiments)
  • SAR: 1 W/kg (for additional experiments)
Exposure 3: 27.12 MHz
Modulation type: AM
Exposure duration: continuous for 1 h/day, 3 h/day or 6 h/day for 7 days or 3 h/day for 3 days
breast tumor-specific modulation frequencies
  • SAR: 0.03 W/kg (average at the monolayer)
  • SAR: 0.05 W/kg (for additional experiments)
  • SAR: 0.1 W/kg (for additional experiments)
  • SAR: 1 W/kg (for additional experiments)
Exposure 4: 27.12 MHz
Modulation type: AM
Exposure duration: continuous for 1 h/day, 3 h/day or 6 h/day for 7 days or 3 h/day for 3 days
  • SAR: 0.4 W/kg

Exposure 1

Main characteristics
Frequency 27.12 MHz
Type
Waveform
Exposure duration continuous for 1 h/day, 3 h/day or 6 h/day for 7 days or 3 h/day for 3 days
Additional info hepatocellular carcinoma-specific modulation frequencies
Modulation
Modulation type AM
Modulation frequency 410.23 Hz–20.365284 kHz
Exposure setup
Exposure source
  • parallel plate capacitor
Setup four 14 cm x 21 cm parallel plate capacitors each consisting of 3 brass plates connected via a coaxial cable to a signal generator and placed inside an incubator
Sham exposure A sham exposure was conducted.
Parameters
Measurand Value Type Method Mass Remarks
SAR 0.03 W/kg - - - average at the monolayer
SAR 0.05 W/kg - - - for additional experiments
SAR 0.1 W/kg - - - for additional experiments
SAR 1 W/kg - - - for additional experiments

Exposure 2

Main characteristics
Frequency 27.12 MHz
Type
Waveform
Exposure duration continuous for 1 h/day, 3 h/day or 6 h/day for 7 days or 3 h/day for 3 days
Additional info randomly chosen frequencies
Modulation
Modulation type AM
Modulation frequency 504.28 Hz–22.401812 kHz
Exposure setup
Exposure source
Sham exposure A sham exposure was conducted.
Parameters
Measurand Value Type Method Mass Remarks
SAR 0.03 W/kg - - - average at the monolayer
SAR 0.05 W/kg - - - for additional experiments
SAR 0.1 W/kg - - - for additional experiments
SAR 1 W/kg - - - for additional experiments

Exposure 3

Main characteristics
Frequency 27.12 MHz
Type
Waveform
Exposure duration continuous for 1 h/day, 3 h/day or 6 h/day for 7 days or 3 h/day for 3 days
Additional info breast tumor-specific modulation frequencies
Modulation
Modulation type AM
Modulation frequency 181.821 Hz–19.406211 kHz
Exposure setup
Exposure source
Sham exposure A sham exposure was conducted.
Parameters
Measurand Value Type Method Mass Remarks
SAR 0.03 W/kg - - - average at the monolayer
SAR 0.05 W/kg - - - for additional experiments
SAR 0.1 W/kg - - - for additional experiments
SAR 1 W/kg - - - for additional experiments

Exposure 4

Main characteristics
Frequency 27.12 MHz
Type
Waveform
Exposure duration continuous for 1 h/day, 3 h/day or 6 h/day for 7 days or 3 h/day for 3 days
Additional info it is not specified clearly in the article whether the modulation frequencies from Exposure 1, 2 and 3 were used here also or not
Modulation
Modulation type AM
Exposure setup
Exposure source
Setup two TEM cells placed inside an incubator; 2 x 6 tissue culture dishes (à 35 mm) per TEM cell
Sham exposure A sham exposure was conducted.
Parameters
Measurand Value Type Method Mass Remarks
SAR 0.4 W/kg - - - -

Reference articles

Exposed system:

Methods Endpoint/measurement parameters/methodology

Investigated system:
Time of investigation:
  • during exposure
  • after exposure

Main outcome of study (acc. to author)

The growth of hepatocellular carcinoma and breast cancer cells was significantly decreased by hepatocellular carcinoma- and breast cancer-specific modulation frequencies, respectively. However, the same frequencies did not affect cell proliferation of non-malignant hepatocytes or normal breast epithelial cells. Inhibition of hepatocellular carcinoma cell proliferation was associated with downregulation of XCL2 and PLP2. Furthermore, hepatocellular carcinoma-specific modulation frequencies disrupted the mitotic spindle.
These data uncovered a novel mechanism controlling the growth of cancer cells at specific modulation frequencies without affecting normal tissues, which may have broad implications in oncology.

Study character:

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