Mechanisms, models and risks of radiation carcinogenesisMecanismos, modelos y riesgos de la carcinogénesis por radiación

Radiation carcinogenesis is an extremely complex phenomenon that progresses over time in a staged and successive manner. The progressive nature of human cancer is now well established. Atypical proliferation,in situ carcinoma, invasive cancer and metastatic dissemination are the main stages of its development. From a molecular standpoint, the basic mechanism of carcinogenesis includes the activation of oncogenes, the inactivation of suppressor genes and, very probably, the involvement of genes related to apoptosis. In radiation carcinogenesis, the Moolgavkar-Knudson (M-K) two-stage clonal expansion model proposes that radiation can act not only as an initiator but also as a promoter of neoplastic transformation, and the Mendelsohn-Pierce (M-P) model postulates that the induction of solid cancer result from the random, and successive, accumulation of mutations at specificloci of the cell genome. According to the latter hypothesis, radiation acts as a general mutagenic agent capable of producing any of these mutations, with a dose-dependent probability proportional to that of their spontaneous occurrence. In contrast to previous assumptions, the M-P model predicts that the age at the time of exposure and the time elapsed since radiation exposure exert little influence on the subsequent development of cancer. According to the best estimates, the risk of cancer from exposure to low radiation doses is 5.10−5 per millisievert of equivalent absorbed dose. Considered overall, the carcinogenetic potential of radiation can be regarded as weak.