The results obtained with DNA-PK-deficient M059J cells and with DNA-PK-proficient M059K cells treated with wortmannin, an inhibitor of DNA-PK and ATM, suggest that the elimination of DNA-PK-dependent non-homologous end-joining can recruit a slow, error-prone repair process, which is DNA-PK independent and favours the increased formation of chromosome aberrations. The nature of this pathway and the way of its participation in aberration formation need further elucidation.

Background: Due to the increasingly common use of endocrine therapy in adjuvant and palliative therapy of breast cancer, a significant number of patients will be treated with radiation therapy and Tamoxifen (TMX) at the same time. Methods: MCF-7 breast cancer cells, cultured by standard methods, were treated with varying doses of TMX or estrogen (ES) and/or graded doses of X-rays. The effects were measured by a clono-genic survival assay. Results: We found a marked decrease in the radiosensitivity of MCF-7 cells which were treated with TMX. This effect was time- and concentration-dependent, with a maximum at a 72-hour incubation. Treatment of the cells with estrogen (ES) increased their radiosensitivity at very high ES doses only. Conclusion: For patients treated with radiotherapy and TMX simultaneously, a negative effect can not be excluded.

In the three cell lines no radiosensitizing effect of paclitaxel could be demonstrated unambiguously. The use of asynchronized cells or the support of cellular repair mechanisms while the cells are blocked in G2/M could partly explain the results.

Multimodal treatment for rectal cancer including RCT leads to hormone level changes and to impaired QoL and sexual functioning. However, because there was no apparent correlation between the analyzed parameters, QoL is probably also influenced by other factors, e.g., psychosocial aspects.

rHuKGF has been shown to ameliorate the radiation tolerance of normal epithelia. The minimum in vitro tumour cell response to rHuKGF compared with normal epithelial cells suggests a potential for selective protection of normal epithelia during radiotherapy. The low FGFR2 expression as well as the FGF7 expression in the tumour cells may contribute to their resistance to rHuKGF treatment.