Introduction to Radiation Biology When Treating Hyperproliferative Benign Diseases

Fig. 45.1

Model of target cells and involved factors. Advanced model of target cells and factors involved in the therapeutic modulation of hyperproliferative/fibrotic benign diseases by a low-dose radiation therapy. Upon fibrotic activation by TGF-β1 and other factors, progenitor fibroblasts will be activated to form myofibroblast/fibrocyte that in turn increase deposition of ECM compounds. Ionizing radiation may interfere with this process by eliminating radiosensitive mitotic fibroblasts, forcing differentiation of fibroblasts, induction of free radicals, modulation of cytokine production and endothelial cell and macrophage activity. Abbreviations are given in the text

Acknowledgements and Conflict of Interest Statement

This work has received funding from the European Atomic Energy Community’s Seventh Framework Programme under grant agreement no FP7-249689 (European Network of Excellence, DoReMi) and the German Federal Ministry of Education and Research (GREWIS, 02NUK017F). The authors have no conflict of interest to declare.

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