## 3 Results
Aberrations, such as a dicentric chromosome, or a ring with an acentric fragment, or a reciprocal translocation, permit the continuation of cell proliferation with the over expression of truncated oncogene which leads to oncogenic transformation. For example, rearrangements of the RET (rearranged during transfection) gene are observed in papillary thyroid carcinoma. Studies conducted after the CNPP accident show a sharp increase in the incidence of pediatric thyroid papillary cancer [83]. Examining the human breast tissue after its irradiation with very low doses (a few mGy) of IR, one may detect, except for induced DSBs, changes in the transcription level of genes [84]. Female breast tissue is proved to be very sensitive to radiation due to the presence of reproductive hormones, including estrogens; the latter may function as carcinogens since they energize the estrogen receptor-mediated cell proliferation [85]. [PERSON] et al. investigated the irradiation of glandular epithelial cells of breast tissue in the dose range representative for mammography screening, with results indicating the existence of a hypersensitive response for DSB induction [86]. In a previous study, they showed that the number of mammography-induced DSBs resulted in chromosomal aberrations, which are a hallmark for cancer [87]. Other studies demonstrated that for very low doses of IR, the \(\gamma\)H2 AX foci induction is much higher than at higher doses [88; 89; 90]. Another effect which plays a key role in the IR-induced carcinogenesis is the bystander effect; this is more relevant to low-dose radiation [91]. At low doses of IR, the response to radiation becomes important in regard to how dominant and extended the bystander effect is in the vicinity of the irradiated cell, and the consequences this will have. Thus, the IR-induced genomic instability and the consequences of the bystander effects indicate a non-linear behavior in the low-dose area. The evidence arising from the published data indicate that the cellular response to low-dose IR is a complex interaction of various modulating factors [92]. [PERSON] and [PERSON] recently attempted to identify the lowest IR dose causing molecular changes in the human body [93]. They concluded that, although the extent of DSBs formation differed depending on the irradiated cell species that were investigated, the lowest limit at which these DNA lesions are formed is approximately 1 mGy. [PERSON] et al. indicated that blood doses ranging between 0.22 and 1.22 mGy may induce somatic DNA lesions, one hour after C.T. examination [94]. Additionally, [PERSON] et al. [95] showed that a very low blood dose 0.15 mGy caused DSBs five minutes after the C.T. examination. An increase in leukemia risk is suggested in children under five years old who were exposed to radioactive fallout from nuclear weapons testing (estimated fallout marrow dose: 1.5 mGy) [96]. According to all the aforementioned data, exposure of an individual to the dose of the underground caesium-137 in areas of such values of surface activity for a period not more than a week, seems to be of very low risk for any future health problems. It would be interesting to investigate the same cases but in a more extended exposure time to IR. In order to study the absorbed dose as a function of the exposure time, we have calculated its values for the deposition density of 3700 kBq\(\cdot\)m\({}^{-2}\) (in the near zone of the nuclear accident) at the exposure times of one day, one week and one month through MCNP code (Figure 4). It is of note that there is an exponential decrease (for the exposure time of one month) in the absorbed dose with the increase in height from the ground (source), while in shorter time periods the curve is converted to a nearly stable line and, simultaneously, a linear increase in this dose with the increase in exposure time. As can be seen in Figure 5, the same trends have the estimated DSBs and SSBs per cell as a function of height and exposure time, correspondingly.