Lack of effect of extremely low frequency electromagnetic fields on cyclin-dependent kinase 4 inhibitor gene p18(INK4C) in electric energy workers.
BACKGROUND
Long-term exposure to extremely low frequency magnetic fields (ELF-MFs) may be a risk factor for human cancer. One mechanism through which ELF-MFs could influence neoplastic development is the deletion/mutation of cancer-related genes. Cellular proliferation follows an orderly progression through the cell cycle, which is governed by different cyclins and cyclin-dependent kinase inhibitors (CDKIs). The putative tumor suppressor gene p18(INK4C) encodes a specific inhibitor of cyclin D-cyclin-dependent kinase 4 inhibitor complexes having an important role in cell-cyclin regulation. It has been found to be deleted/mutated in a variety of human cancers. Therefore, this study is to investigate whether or not long-term extremely low frequency electromagnetic field exposure may be a risk factor for human cancer due to the gene p18(INK4C) deletion/mutation.


METHODS
The study was carried out on 31 male electric workers and 30 healthy males between 30 and 40 years of age from the same geographic area and with similar lifestyles. We studied both groups by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP).


RESULTS
In comparison to the controls, band migration of exon 1 was found to be indifferent in all the subjects tested. However, only exon 2 of two electric workers was slow in migration with respect to both control and other subjects in the same class. This slow migration suggests that point mutations or polymorphisms may exist in this region of the p18(INK4C) gene. The relative risk (RR) for the unmatched analysis was 1,069 (95% confidence interval [CI] 0.975-1.172).


CONCLUSIONS
The results suggest that long-term ELF-MFs exposure does not significantly increase the risk of cancer.
Erdal
Nurten
N
Department of Biophysics, Faculty of Medicine, University of Mersin, Mersin, Turkey. nerdal@mersin.edu.tr
Erdal
Mehmet Emin
ME
Gürgül
Serkan
S
D000328:Adult; D018797:Cell Cycle Proteins / Q000235:genetics*; D051358:Cyclin-Dependent Kinase 4; D050763:Cyclin-Dependent Kinase Inhibitor p18; D018844:Cyclin-Dependent Kinases / Q000037:antagonists & inhibitors*; D004574:Electromagnetic Fields; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics*; D008297:Male; D009369:Neoplasms / Q000235:genetics; D016273:Occupational Exposure; D009790:Occupations; D017354:Point Mutation; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D018807:Polymorphism, Single-Stranded Conformational; D011210:Power Plants; D011518:Proto-Oncogene Proteins / Q000037:antagonists & inhibitors*; D012307:Risk Factors; D025521:Tumor Suppressor Proteins / Q000235:genetics*
C493971:CDKN2C protein, human; D018797:Cell Cycle Proteins; D050763:Cyclin-Dependent Kinase Inhibitor p18; D047908:Intracellular Signaling Peptides and Proteins; D011518:Proto-Oncogene Proteins; D025521:Tumor Suppressor Proteins; C015482:protein kinase modulator; C495900:CDK4 protein, human; D051358:Cyclin-Dependent Kinase 4; D018844:Cyclin-Dependent Kinases