Meta-analysis of non-tumour doses for radiation-induced cancer on the basis of dose-rate

Purpose: Quantitative analysis of cancer risk of ionising radiation as a function of dose-rate

Radiation-induced versus endogenous DNA damage: commentary on Pollycove and Feinendegen

Quantitative comparison of ROS-induced endogenous DNA damage with DNA damage induced by ionizing radiation at environmental level, presented by Pollycove and Feinedegen, is timely and provides basic date for establishing a a sound rule for radiation protection. Main point added to their estimation is quantitative data on oxidative damage to DNA precursormolecules, such as oxo dGTP and their cellular decomposition efficiency. If the precursor damages are taken into accout, the amount of initial endogenous DNA damage would be increased by a factor of 100-10000

Threshold dose problems in radiation carcinogenesis: A review of non-tumor doses

Non-tumour-inducing doses exist in dose-response data on experimental animals and humans, although a linear non-threshold model has been adopted for estimating cancer risk of ionising radiation at a low dose region for radiation protection purposes. Here, data on non- tumour dose, Dnt, the maximum dose at which a statistically significant increase of tumours is not observed, were reviewed in the literature. Dnt values range from 0.1 to 3 Gy for a variety of tumours induced by acute whole-body irradiation at low LET. This becomes one order higher by fractionation of radiation dose and further by extending irradiation chronically. Non-tumour doses for irradiation of a part of the body are one order higher than those for whole-body irradiation, indicating a higher tolerance level in the partial-body irradiation. Tumour data with high LET radiation also show non-tumour dose and its decrease at a very low dose rate. The variation of Dnt is explained by the host tolerance, including inducible and non-inducible DNA repair, apoptotic elimination of unrepaired cells, and immunological suppression of tumour development

X chromosome inactivation-mediated cellular mosaicism for the study of the monoclonal origin and recurrence of mouse tumors: a review

X chromosome inactivation-mediated cellular mosaicism was applied to study the clonal nature of experimental and human tumors and to judge whether apparently recurrent tumors which appear after therapeutic treatment are truly due to recurrence or due to new induction of a second tumor. Results show that the majority of experimental and human tumors, including benign tumors, are monoclonal and that the majority of apparently recurrent tumors are due to true recurrence. A series of experimental studies on this topic are reviewed