1 mW/kg. We had previously hypothesized that the mechanism of action of electromagnetic fields amplitude-modulated at insomnia-specific frequencies was due to modification in ions and neurotransmitters[6], as see more demonstrated in animal models[16], as such biological effects had been reported at comparable SARs. However, this hypothesis does not provide a satisfactory explanation for the clinical results observed in patients with advanced cancer. First, the levels of electromagnetic fields delivered to organs such as the liver, adrenal gland, prostate and hip bones, are substantially

lower than the levels delivered to the head. Second, there is currently no acceptable rationale for a systemic anti-tumor effect that would involve subtle changes in neurotransmitters and ions within the central nervous system. Consequently, we hypothesize that the systemic changes (pulse amplitude, blood pressure, skin resistivity) observed while patients are exposed to tumor-specific frequencies are the reflection of a systemic effect generated by these frequencies. These observations suggest that electromagnetic fields, which are amplitude-modulated

at tumor-specific frequencies, do not act solely on tumors but may have wide-ranging buy Mocetinostat effects on tumor host interactions, e.g. immune modulation. The exciting results from this study provide a strong rationale to study the mechanism of action of tumor-specific frequencies in vitro and in Anacetrapib animal models, which may lead

to the discovery of novel pathways controlling cancer growth. Acknowledgements The authors would like to thank Al B. Benson, III, Northwestern University and Leonard B. Saltz, Memorial Sloan-Kettering Cancer Center for providing insightful comments and reviewing the manuscript. Neither of them received any compensation for their work. Presented in part: abstract (ID 14072) ASCO 2007; oral presentation (29th Annual Meeting of the Bioelectromagnetics Society, Kanazawa, Japan, 2007). Funding: study funded by AB and BP. The costs associated with the design and engineering of the devices used in this study were paid by AB and BP. BB and RM did not receive any compensation for their independent review of the imaging studies. References 1. Reite M, Higgs L, Lebet JP, Barbault A, Rossel C, Kuster N, Dafni U, Amato D, Pasche B: Sleep Inducing Effect of Low Energy Emission Therapy. Bioelectromagnetics 1994, 15: 67–75.CrossRefPubMed 2. Lebet JP, Barbault A, Rossel C, Tomic Z, Reite M, Higgs L, Dafni U, Amato D, Pasche B: Electroencephalographic changes following low energy emission therapy. Ann Biomed Eng 1996, 24: 424–429.CrossRefPubMed 3. Higgs L, Reite M, Barbault A, Lebet JP, Rossel C, Amato D, Dafni U, Pasche B: Subjective and Objective Poziotinib Relaxation Effects of Low Energy Emission Therapy. Stress Medicine 1994, 10: 5–13.CrossRef 4. Pasche B, Erman M, Mitler M: Diagnosis and Management of Insomnia. N Engl J Med 1990, 323: 486–487.CrossRef 5.