Modulation of Exposure to Static Magnetic Field Affects Targeted Therapy of Solid Tumors In Vivo

Anticancer Res. 2018 Aug;38(8):4549-4555. doi: 10.21873/anticanres.12759.

Abstract

Background: Static magnetic fields (SMF) exhibit antitumoral activity and enhance the efficacy of chemotherapy by opening the tumor-blood barrier. This study aimed to analyze different SMF-exposure protocols on epidermal growth factor receptor (EGFR)-overexpressing tumors, as well as their combination with cetuximab.

Materials and methods: Experiments were performed in skinfold chamber preparations of C57Bl/6-and CD-1nu/nu mice bearing LLC-1 tumors. Animals were exposed to 587 mT magnetic field following different exposure protocols. A subgroup received additional cetuximab injections. Using in vivo-fluorescence microscopy and planimetry, tumor angiogenesis, growth and microcirculation were repeatedly analyzed for 13 days.

Results: In contrast to daily short SMF exposure, three-fold SMF exposure for 2 h led to a significant 46% reduction of tumor growth. Adding cetuximab to SMF exposure did not yield any benefit, although cetuximab monotherapy was highly effective (53% reduction of tumor growth), indicating a potential interference of SMF and EGFR signaling. No effects on microcirculation, angiogenesis or leukocyte-endothelium interactions were documented.

Conclusion: The use of SMF is promising in the treatment of solid tumors; however, it appears to interfere with EGFR-targeted therapy.

Keywords: EGFR; Squamous cell carcinoma; static magnetic field; targeted therapy.

MeSH terms

  • Animals
  • Cell Proliferation / drug effects
  • Cetuximab / pharmacology*
  • Endothelium / drug effects
  • Endothelium / metabolism
  • ErbB Receptors / metabolism
  • Leukocytes / drug effects
  • Leukocytes / metabolism
  • Magnetic Fields
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Nude
  • Microcirculation / drug effects
  • Neoplasms / drug therapy*
  • Neoplasms / metabolism
  • Neovascularization, Pathologic / drug therapy
  • Neovascularization, Pathologic / metabolism

Substances

  • ErbB Receptors
  • Cetuximab