Oxygen Enhancement Ratio of Proton Beams: The Precise Report of the Same Institution’s Experiments Using the Clinical Equipments

Abstract

(sensitive versus resistant/metastasis) are used to identify pathways involved in radiation escape. Results: Radiation escape has been proven by growth delay assays (p<0.05) and earlier onset of metastatic spread (p<0.05) to primarily the lungs. In addition, we observed that the pre-irradiated tumors were significantly less sensitive for topotecan and olaparib compared to the response of naive tumors (p<0.05). In contrast, radioresistant tumors did not respond differently to cisplatin or docetaxel. Althoughwe know that loss of 53BP1 (and restoration of RAD51 foci) can cause olaparib resistance in this tumor model, this only explained very few cases of the radioresistant tumors. Conclusions: Tumors which escape from fractionated radiation therapy show different radiation and systemic treatment responses. These phenomena are likely due to specific characteristics in the DNA damage repair pathway induced or selected by the fractionated irradiation. Ongoing RNAseq and DNA exome sequencing may reveal new targets to overcome radiation escape and will help to answer the question whether these cellular characteristics are acquired or selected during the fractionated treatment. We hope that this model and high precision radiation therapy will contribute to novel and clinically relevant insights into basic mechanisms of radiation escape. Author Disclosure: G. Borst: None. M. Barazas: None. A. Gasparini: None. W. Sol: None. J. Jonkers: None. M. Verheij: None. J. Sonke: None. S. Rottenberg: None.