# Treatment of glioblastoma with tumor-specific amplitude-modulated radiofrequency electromagnetic fields

**Authors:** Hugo Jimenez, Denise Gibo, Sambad Sharma, Michael Pennison, Lance D. Miller, Minghui Wang, Kimberly Sheffield, Liyue Zhang, Allan Johansen, Preeya Achari, Callum Mcgrath, Sean Lester, Jason Tang, Kojo Agyemang, Annette Johnson, Christopher T. Whitlow, Michael Chan, Kounosuke Watabe, Ralph D’Agostino, Janaka Liyanage, Asfar Azmi, Geoffrey Barger, Alexandre Barbault, Glenn J. Lesser, Waldemar Debinski, Boris C. Pasche

PMC · DOI: 10.18632/oncotarget.28770 · Oncotarget · 2025-10-13

## TL;DR

This study explores using specific radiofrequency electromagnetic fields to treat glioblastoma, showing both lab and early patient results.

## Contribution

The first report of GB-specific AM RF EMF inhibiting GB cell proliferation and showing clinical feasibility in brain tumor patients.

## Key findings

- GBMF inhibited proliferation of several glioblastoma cell lines.
- GBMF disrupts the mitotic spindle via the Polo-Like Kinase pathway.
- Clinical and radiological benefits observed in a patient with recurrent glioblastoma.

## Abstract

Background: Intrabuccal administration of amplitude-modulated 27.12 MHz radiofrequency electromagnetic fields (AM RF EMF) resulting in the systemic delivery of low and safe levels of AM RF EMF has shown activity in several forms of cancer.

Methods: Glioblastoma (GB) cell lines were exposed to GB-specific AM RF EMF (GBMF) three hours per day at a level of exposure identical to patients during treatment. Cellular assays and agnostic genomic approaches were used to characterize the mechanism-of-action. One patient with therapy refractory GB received compassionate use treatment with GBMF as well as a second patient with refractory oligodendroglioma.

Results: Treatment with GBMF inhibited the proliferation of several GB cell lines. CACNA1H mediates the effect of GBMF. GBMF modulates the “Mitotic Roles of Polo-Like Kinase” pathway resulting in the disruption of GB mitotic spindle. There was evidence of clinical and radiological benefit in a 38-year-old patient with recurrent GB and evidence of safety and feasibility in a 47-year-old patient with oligodendroglioma.

Conclusions: This is the first report showing in vitro antitumor activity, disruption of the mitotic spindle, activation of the Mitotic Roles of Polo-like kinase pathway in GB. This is also the first report showing feasibility and clinical activity in patients with brain tumor.

## Linked entities

- **Genes:** CACNA1H (calcium voltage-gated channel subunit alpha1 H) [NCBI Gene 8912]
- **Diseases:** glioblastoma (MONDO:0018177), oligodendroglioma (MONDO:0002540)

## Full-text entities

- **Genes:** PLK1 (polo like kinase 1) [NCBI Gene 5347] {aka PLK, STPK13}, CACNA1H (calcium voltage-gated channel subunit alpha1 H) [NCBI Gene 8912] {aka CACNA1HB, Cav3.2, ECA6, EIG6, HALD4}
- **Diseases:** cancer (MESH:D009369), brain tumor (MESH:D001932), GB (MESH:D005909), oligodendroglioma (MESH:D009837)
- **Chemicals:** AM RF EMF (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12517218/full.md

## References

35 references — full list in the complete paper: https://tomesphere.com/paper/PMC12517218/full.md

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Source: https://tomesphere.com/paper/PMC12517218