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Additional file 1: Figure S1. Kinetics of the γH2AX foci in excess in fibroblasts after a single helical head CT scan (a), or a double-helical head CT scan (b) at the indicated post-irradiation times (t0 = non-irradiated). Data result from those shown in Fig. 2 with background subtraction in order to show γH2AX foci in excess effectively due to CT exposure. Error bars indicate SEM. Figure S2. Kinetics of pATM foci in excess in fibroblasts (a) after a single helical head CT scan, (b) or a double-helical head CT scan at the indicated post-irradiation times (t0 = non irradiated). Data result from those shown in Fig. 3 with background subtraction in order to show γH2AX foci in excess effectively due to CT exposure. Error bars indicate SEM. Figure S3. Kinetics of γH2AX foci in excess in astrocytes (a) after a single helical head CT scan, or (b) a double-helical head CT scan at the indicated post-irradiation times (t0 = non-irradiated). Data result from those shown in Fig. 4 with background subtraction in order to show γH2AX foci in excess effectively due to CT exposure. Error bars indicate SEM. Figure S4. Kinetics of the pATM foci in in excess astrocytes (a) after a single helical head CT scan, or (b) a double-helical head CT scan at the indicated post-irradiation times (t0 = non-irradiated). Data result from those shown in Fig. 5 with background subtraction in order to show γH2AX foci in excess effectively due to CT exposure. Error bars indicate SEM. Figure S5. Distribution of the number of γH2AX foci per cell over the 300 nuclei scored for the 200CLB and 85MA cell lines at 1h after a single-helical head CT exposure. Table S1. Statistical results and p-values

Purpose: Xeroderma Pigmentosum (XP) is a rare, recessive genetic disease associated with photosensitivity, skin cancer proneness, neurological abnormalities and impaired nucleotide excision repair of the UV-induced DNA damage. Less frequently, XP can be associated with sensitivity to ionizing radiation (IR). Here, a complete radiobiological characterization was performed on a panel of fibroblasts derived from XP-group D patients (XPD). Materials and methods: Cellular radiosensitivity and the functionality of the recognition and repair of chromosome breaks and DNA double-strand breaks (DSB) was evaluated by different techniques including clonogenic cell survival, micronuclei, premature chromosome condensation, pulsed-field gel electrophoresis, chromatin decondensation and immunofluorescence assays. Quantitative correlations between each endpoint were analyzed systematically. Results: Among the seven fibroblast cell lines tested, those derived from three non-relative patients holding the p.[Arg683Trp];[Arg616Pro] XPD mutations showed significant cellular radiosensitivity, high yield of residual micronuclei, incomplete DSB recognition, DSB and chromosome repair defects, impaired ATM, MRE11 relocalization, significant chromatin decondensation. Interestingly, XPD transduction and treatment with statins and bisphosphonates known to accelerate the radiation-induced ATM nucleoshuttling led to significant complementation of these impairments. Conclusions: Our findings suggest that some subsets of XPD patients may be at risk of radiosensitivity reactions and treatment with statins and bisphosphonates may be an interesting approach of radioprotection countermeasure. Different mechanistic models were discussed to better understand the potential specificity of the p.[Arg683Trp];[Arg616Pro] XPD mutations.