The importance of bystander effects in radiation therapy in melanoma skin-cancer cells and umbilical-cord stromal stem cells

摘要: Purpose: To examine direct and bystander radiation-induced effects in normal umbilical-cord stromal stem cell (HCSSC) lines human cancer cells. Materials methods: The UCSSC used this study were obtained our laboratory. Two (UCSSC 35 37) two melanoma skin-cancer cells (A375 G361) exposed to ionizing radiation measure acute radiation-dosage cell-survival curves cell-death response. Results: Normal cells, although extremely sensitive radiation, resistant the effect whilst tumor irradiated cell-conditioned media, showing a dose–response relationship that became saturated at relatively low doses. We applied biophysical model describe through binding of ligand This allowed us calculate maximum death ( vmax) produced by together with its association constant (KBy) terms dose equivalence (Gy). values for KBy A375 G361 0.23 0.29 Gy, respectively. Conclusion: Our findings help understand how anticancer therapy could have an additional decisive response sub-lethally hit damage might be required successful because survival communicating is reduced. 2011 Elsevier Ireland Ltd. All rights reserved. Radiotherapy Oncology 102 (2012) 450–458 Variation intrinsic radiosensitivity both human-tumor normal-tissue already recognized, these differences may related clinical curability tolerance treatment [1]. At present, choice appropriate all patients based on balance between minimizing incidence severe normaltissue complications maximizing probability local control. Radiation unusual toxic agent timing tissue can vary widely from one patient next [2,3]. traditional radiobiological models, which assumed result cascade simultaneous or successive events start initial DNA. Radiation-induced lethal potentially DNA explained linear-quadratic also total isoeffective per fraction fractionated [4]. Based control requires clonogenic receive dose. [5] biological indicator quantity energy transferred Nevertheless, late still not been fully thus more general theory consequences appears necessary [6]. A key consequence occurs within nucleus, producing range lesions, double-strand breaks (DSBs) play vital role determining whether they survive exposure [7]. presence activates repair mechanisms as well signal transduction pathways, leading cycle arrest apoptosis. suppressor protein p53 plays arrested apoptosis ensues after genotoxic attack. Parp-1 participates following irradiation [8,9], but events, including intra- inter-cellular signaling involving free radicals, reactive oxygen species, cytokines epigenetic changes, has clarified results