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• W2067331906 abstract "Purpose/Objective(s)Repair of sublethal damage (SLD) during protracted dose delivery may potentially influence the biological effect of intraoperative radiotherapy (IORT) with low-energy x rays. The purpose was to determine experimental halftimes of SLD repair for cell inactivation in vitro and compare it with repair of DNA damage in the same dose range.Materials/MethodsSLD repair was detected by split-dose recovery for colony formation of Chinese hamster V79 and human breast tumor MCF7 cell lines, and for human normal skin fibroblasts (passage 6 - 8). Repair halftimes were derived for the linear-quadratic (L-Q) formalism including the Lea-Catcheside time factor. DNA repair foci were detected by antibodies against γH2AX and 53BP1. Irradiations were performed with 6 MV x rays, or 50 kV x rays from a surface radiotherapy machine (Dermopan, Siemens) or a miniaturized x ray machine for IORT (Intrabeam, Carl Zeiss Surgical GmbH).ResultsThe V79 and MCF7 cell lines showed split-dose recovery indicating SLD repair for 2x6 Gy or 2x4 Gy (yielding surviving fractions, SF ∼ 0.004 - 0.006 for single total-dose irradiation). The SLD repair halftime for split-dose intervals up to 40 min increased from 15 to 25 min for V79, but was constant at 39 min for MCF7. Skin fibroblasts showed no SLD repair up to 6 h post-irradiation which was associated with absence of a shoulder on the survival curve. SLD repair was validated for split-dose irradiation with 50 kV x rays from Dermopan, using V79 cells. The kinetics of induction and decay of γH2AX foci after acute irradiation was similar in all three cell types with rapid induction to a maximum at 30 min post irradiation followed by a decay, and with few residual foci at 24 h. The maximum number of foci produced by 4.7 Gy of 50 kV x rays from Intrabeam at the highest dose rate in air (∼0.42 Gy/min) was comparable to 6 Gy of 6 MV x rays (6 Gy/min) consistent with an RBE ∼1.3 but decreased at larger distances as the total irradiation time increased. The dose-response for 53BP1 in fibroblasts suggested efficient repair at low doses (0 - 2 Gy) but increasing saturation at higher doses (8 - 16 Gy).ConclusionsThe repair halftime for the breast cancer cell line was comparable with the duration of IORT. Thus SLD repair is relevant for protracted dose delivery during IORT with 50 kV x rays and should be included when modeling RBE and clinical outcome. DNA repair proficiency of the skin fibroblast strain in the absence of SLD repair suggested that DNA repair foci are unlikely to represent SLD. Although evidence exists that the clinical risk of late reaction may be determined primarily by other factors than cellular radiosensitivity of fibroblasts, the present findings could be important for the mechanistic interpretation of the L-Q formalism. Purpose/Objective(s)Repair of sublethal damage (SLD) during protracted dose delivery may potentially influence the biological effect of intraoperative radiotherapy (IORT) with low-energy x rays. The purpose was to determine experimental halftimes of SLD repair for cell inactivation in vitro and compare it with repair of DNA damage in the same dose range. Repair of sublethal damage (SLD) during protracted dose delivery may potentially influence the biological effect of intraoperative radiotherapy (IORT) with low-energy x rays. The purpose was to determine experimental halftimes of SLD repair for cell inactivation in vitro and compare it with repair of DNA damage in the same dose range. Materials/MethodsSLD repair was detected by split-dose recovery for colony formation of Chinese hamster V79 and human breast tumor MCF7 cell lines, and for human normal skin fibroblasts (passage 6 - 8). Repair halftimes were derived for the linear-quadratic (L-Q) formalism including the Lea-Catcheside time factor. DNA repair foci were detected by antibodies against γH2AX and 53BP1. Irradiations were performed with 6 MV x rays, or 50 kV x rays from a surface radiotherapy machine (Dermopan, Siemens) or a miniaturized x ray machine for IORT (Intrabeam, Carl Zeiss Surgical GmbH). SLD repair was detected by split-dose recovery for colony formation of Chinese hamster V79 and human breast tumor MCF7 cell lines, and for human normal skin fibroblasts (passage 6 - 8). Repair halftimes were derived for the linear-quadratic (L-Q) formalism including the Lea-Catcheside time factor. DNA repair foci were detected by antibodies against γH2AX and 53BP1. Irradiations were performed with 6 MV x rays, or 50 kV x rays from a surface radiotherapy machine (Dermopan, Siemens) or a miniaturized x ray machine for IORT (Intrabeam, Carl Zeiss Surgical GmbH). ResultsThe V79 and MCF7 cell lines showed split-dose recovery indicating SLD repair for 2x6 Gy or 2x4 Gy (yielding surviving fractions, SF ∼ 0.004 - 0.006 for single total-dose irradiation). The SLD repair halftime for split-dose intervals up to 40 min increased from 15 to 25 min for V79, but was constant at 39 min for MCF7. Skin fibroblasts showed no SLD repair up to 6 h post-irradiation which was associated with absence of a shoulder on the survival curve. SLD repair was validated for split-dose irradiation with 50 kV x rays from Dermopan, using V79 cells. The kinetics of induction and decay of γH2AX foci after acute irradiation was similar in all three cell types with rapid induction to a maximum at 30 min post irradiation followed by a decay, and with few residual foci at 24 h. The maximum number of foci produced by 4.7 Gy of 50 kV x rays from Intrabeam at the highest dose rate in air (∼0.42 Gy/min) was comparable to 6 Gy of 6 MV x rays (6 Gy/min) consistent with an RBE ∼1.3 but decreased at larger distances as the total irradiation time increased. The dose-response for 53BP1 in fibroblasts suggested efficient repair at low doses (0 - 2 Gy) but increasing saturation at higher doses (8 - 16 Gy). The V79 and MCF7 cell lines showed split-dose recovery indicating SLD repair for 2x6 Gy or 2x4 Gy (yielding surviving fractions, SF ∼ 0.004 - 0.006 for single total-dose irradiation). The SLD repair halftime for split-dose intervals up to 40 min increased from 15 to 25 min for V79, but was constant at 39 min for MCF7. Skin fibroblasts showed no SLD repair up to 6 h post-irradiation which was associated with absence of a shoulder on the survival curve. SLD repair was validated for split-dose irradiation with 50 kV x rays from Dermopan, using V79 cells. The kinetics of induction and decay of γH2AX foci after acute irradiation was similar in all three cell types with rapid induction to a maximum at 30 min post irradiation followed by a decay, and with few residual foci at 24 h. The maximum number of foci produced by 4.7 Gy of 50 kV x rays from Intrabeam at the highest dose rate in air (∼0.42 Gy/min) was comparable to 6 Gy of 6 MV x rays (6 Gy/min) consistent with an RBE ∼1.3 but decreased at larger distances as the total irradiation time increased. The dose-response for 53BP1 in fibroblasts suggested efficient repair at low doses (0 - 2 Gy) but increasing saturation at higher doses (8 - 16 Gy). ConclusionsThe repair halftime for the breast cancer cell line was comparable with the duration of IORT. Thus SLD repair is relevant for protracted dose delivery during IORT with 50 kV x rays and should be included when modeling RBE and clinical outcome. DNA repair proficiency of the skin fibroblast strain in the absence of SLD repair suggested that DNA repair foci are unlikely to represent SLD. Although evidence exists that the clinical risk of late reaction may be determined primarily by other factors than cellular radiosensitivity of fibroblasts, the present findings could be important for the mechanistic interpretation of the L-Q formalism. The repair halftime for the breast cancer cell line was comparable with the duration of IORT. Thus SLD repair is relevant for protracted dose delivery during IORT with 50 kV x rays and should be included when modeling RBE and clinical outcome. DNA repair proficiency of the skin fibroblast strain in the absence of SLD repair suggested that DNA repair foci are unlikely to represent SLD. Although evidence exists that the clinical risk of late reaction may be determined primarily by other factors than cellular radiosensitivity of fibroblasts, the present findings could be important for the mechanistic interpretation of the L-Q formalism." @default.
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• W2067331906 title "Sublethal Damage (SLD) Repair: Relation to DNA Repair and Implications for Protracted Irradiation with Low-energy X-rays" @default.
• W2067331906 doi "https://doi.org/10.1016/j.ijrobp.2011.06.1271" @default.
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