Microwaves from Mobile Phones Inhibit 53BP1 Focus Formation in Human Stem Cells More Strongly Than in Differentiated Cells: Possible Mechanistic Link to Cancer Risk.
BACKGROUND
It is widely accepted that DNA double-strand breaks (DSBs) and their misrepair in stem cells are critical events in the multistage origination of various leukemias and tumors, including gliomas.


OBJECTIVE
We studied whether microwaves from mobile telephones of the Global System for Mobile Communication (GSM) and the Universal Global Telecommunications System (UMTS) induce DSBs or affect DSB repair in stem cells.


METHODS
We analyzed tumor suppressor TP53 binding protein 1 (53BP1) foci that are typically formed at the sites of DSB location (referred to as DNA repair foci) by laser confocal microscopy.


RESULTS
Microwaves from mobile phones inhibited formation of 53BP1 foci in human primary fibroblasts and mesenchymal stem cells. These data parallel our previous findings for human lymphocytes. Importantly, the same GSM carrier frequency (915 MHz) and UMTS frequency band (1947.4 MHz) were effective for all cell types. Exposure at 905 MHz did not inhibit 53BP1 foci in differentiated cells, either fibroblasts or lymphocytes, whereas some effects were seen in stem cells at 905 MHz. Contrary to fibroblasts, stem cells did not adapt to chronic exposure during 2 weeks.


CONCLUSIONS
The strongest microwave effects were always observed in stem cells. This result may suggest both significant misbalance in DSB repair and severe stress response. Our findings that stem cells are most sensitive to microwave exposure and react to more frequencies than do differentiated cells may be important for cancer risk assessment and indicate that stem cells are the most relevant cellular model for validating safe mobile communication signals.
Markovà
Eva
E
Department of Genetics, Microbiology and Toxicology, Stockholm University, Stockholm, Sweden; Laboratory of Molecular Genetics, Cancer Research Institute, Bratislava, Slovak Republic.
Malmgren
Lars O G
LO
MAX-lab, Lund University, Lund, Sweden.
Belyaev
Igor Y
IY
Department of Genetics, Microbiology and Toxicology, Stockholm University, Stockholm, Sweden; Laboratory of Molecular Genetics, Cancer Research Institute, Bratislava, Slovak Republic; Laboratory of Radiobiology, General Physics Institute, Russian Academy of Science, Moscow, Russia.
D040421:Cell Phone; D053903:DNA Breaks, Double-Stranded; D004260:DNA Repair; D004307:Dose-Response Relationship, Radiation; D005347:Fibroblasts / Q000166:cytology / Q000378:metabolism / Q000528:radiation effects*; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism / Q000528:radiation effects*; D008872:Microwaves / Q000009:adverse effects*; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism / Q000528:radiation effects*; D000071857:Tumor Suppressor p53-Binding Protein 1
D047908:Intracellular Signaling Peptides and Proteins; C498301:TP53BP1 protein, human; D000071857:Tumor Suppressor p53-Binding Protein 1