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Meylan, E., Dooley, A.L., Feldser, D.M., Shen, L., Turk, E., Ouyang, C. and Jacks, T. (2009) Requirement for NF-κB signalling in a mouse model of lung adenocarcinoma. Nature, 462, 104-107. doi:10.1038/nature08462

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• TITLE: Cancer induction pathways and HF-EMF irradiation

  AUTHORS: Gérard Ledoigt, Dominique Belpomme

  KEYWORDS: Cell Membrane; Chronic Inflammation; EMF Exposure; Gene Expression; Cancer; Carcinogenesis; NF-κB

  JOURNAL NAME: Advances in Biological Chemistry, Vol.3 No.2, April 30, 2013

  ABSTRACT: The response of cells to different types of electromagnetic fields can be induced by low-level (athermal) high frequency (HF) electromagnetic field (EMF) exposure associated with mobile phone technologies. There are many examples of biological effects involving the epigenome. EMF could trigger protein activation mediated by ligands, such as Ca2+, that alter the conformation of binding proteins, especially the NADPH plasmic membrane oxidase, so inducing increased formation of reactive oxygen species (ROS) that may alter proteomic functions. Classical antiapoptotic and procarcinogenic signaling mechanisms that are commonly found activated in human malignancies and in inflammation mainly involve the transcription factor NF-κB. The microenvironment that exists during chronic inflammation can contribute to cancer progression. The data support the proposition that long term HF-EMF exposure caused by improper use of cell phones may potentially cause cancer.