It has been known that genome instability exists in many cancers, and it can be a potential cause in tumorigenesis. More and more evidence indicates that genome instability is a crucial step in the tumorigenesis for some cases induced by ionized radiation (Yokota et al., 2010). Thus, it has been proposed in some studies (Oikawa et al., 2011) that by introducing ionized radiation experimentally, those genome instability induced by irradiation can serve as a model for research in radiation related carcinogenesis, which will provide valuable reference for risk evaluation of public health imposed by radiation and for better understanding of radiation related carcinogenesis.
Some detectable biological endpoints have been utilized for genomic studies, such as point mutation, chromosomal rearrangement, micronucleus formation, accelerating cellular differentiation, and decreasing cloning rate (Yokota et al., 2010). However, some of these biological endpoints occur in form of spontaneous mutation, for which a prolonged time period is needed for observation, and their prevalence is too low to study. Thus, difficulties may be encountered when common approaches are used for direct detection of genome instability. In our present study, in light of the hypothesis of second-hit promotion in multiple-stage of carcinogenesis, 60Co- ray induced genome instability has been investigated with introduction of a second irradiation in human normal liver cells, which will render unique evidence experimentally to radiation related studies in the liver and its protection.
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