[en] Purpose: Adjuvant 'whole breast radiotherapy' (WBRT) is the standard of care after breast conserving surgery in women with breast cancer. Throughout different cancer stages the addition of WBRT leads to significantly improved rates of freedom from local failure and overall survival. WBRT is generally well tolerated. A 5-10%-rate of severe acute or long-term side effects is commonly observed. For both radiation-mediated tumor-cell-elimination and induction of side effects, DNA-double-strand-breaks (DSB) presumably play the decisive role. The intensity of normal tissue reactions in radiotherapy can, in part, be attributed to the intrinsic DSB repair-capacity. In this study in vivo and in vitro experiments are carried through in order to assess DSB repair-kinetics in blood lymphocytes of women with breast cancer. These findings are to be correlated with the degree of radiation-induced normal tissue toxicity. Patients and Methods: Eighteen patients with breast cancer, in whom WBRT was indicated, were examined. A total WBRT dose of 50 Gy (single dose 2 Gy) with an additional boost-radiotherapy to the initial tumor-region to a total dose of 60-66 Gy was administered. DSB repair was determined by means of counting γ-H2AX foci in blood lymphocytes at predefined points in time, i.e. before and 0.5 h; 2.5 h; 5 h and 24 h after in vivo irradiation (1st fraction of WBRT) and before and 0.5 h; 2.5 h and 5 h after in vitro irradiation with increasing radiation doses in the range of 10 - 500 mGy. Acute normal tissue toxicity was scored on the basis of a modified RTOG-classification (main aspects were erythema and dry or moist skin desquamation). Results: DSB repair-halflife-times did not differ between patients with a higher or lower than average incidence of acute side effects. In patients with 'above average' side effects larger irradiation volumes were treated (volume surrounded by the 50%-isodose). Adjusted for these, no single patients showed elevated residual γ-H2AX foci 24 h after dose-exposure. Patients with a number of residual γ-H2AX foci after 24 h higher than the average + one standard deviation had an increased risk for the development of a severe radiation-induced dermatitis (n=3). In the in vitro experiments, a linear relationship between applied dose and the γ-H2AX foci count could be demonstrated. The in vitro γ-H2AX foci counts also yield calibration-curves, which allow the assessment of the irradiated proportion of lymphocytes in partial-body radiotherapy. Conclusions: In vivo-determination of DSB repair by means of counting γ-H2AX foci can be applied reliably in a clinical situation characterized by an interindividually different partial-body dose exposure. It allows identification of patients with elevated residual γ-H2AX foci-levels, assumedly indicating an impaired DSB repair. The results, even though showing a trend, do not hint at a close correlation between halflife-times of γ-H2AX foci-elimination or residual γ-H2AX foci after 24 h and the incidence of severe acute toxicity. The interpretation of the results is hindered by the limited number of examined patients.