@article{oai:repo.qst.go.jp:00082094,
 author = {Anne‑SophieWozny and Alphonse, Gersende and Cassard, Audrey and Céline, Malésys and Louati, Safa and Beuve, Michael and Lalle, Philippe and Ardail, Dominique and Nakajima, Tetsuo and Claire, Rodriguez‑Lafrasse and Tetsuo, Nakajima},
 journal = {Scientific Reports},
 month = {Dec},
 note = {DNA double-strand breaks (DSBs) induced by photon irradiation are the most deleterious damage for cancer cells and their efficient repair may contribute to radioresistance, particularly in hypoxic conditions. Carbon ions (C-ions) act independently of the oxygen concentration and trigger complex- and clustered-DSBs difficult to repair. Understanding the interrelation between hypoxia, radiation-type, and DNA-repair is therefore essential for overcoming radioresistance. The DSBs signaling and the contribution of the canonical non-homologous end-joining (NHEJ-c) and homologous-recombination (HR) repair pathways were assessed by immunostaining in two cancer-stem-cell (CSCs) and non-CSCs HNSCC cell lines. Detection and signaling of DSBs were lower in response to C-ions than photons. Hypoxia increased the decay-rate of the detected DSBs (γH2AX) in CSCs after photons and the initiation of DSB repair signaling (P-ATM) in CSCs and non-CSCs after both radiations, but not the choice of DSB repair pathway (53BP1). Additionally, hypoxia increased the NHEJ-c (DNA-PK) and the HR pathway (RAD51) activation only after photons. Furthermore, the involvement of the HR seemed to be higher in CSCs after photons and in non-CSCs after C-ions. Taken together, our results show that C-ions may overcome the radioresistance of HNSCC associated with DNA repair, particularly in CSCs, and independently of a hypoxic microenvironment.},
 title = {Impact of hypoxia on the double-strand break repair after photon and carbon ion irradiation of radioresistant HNSCC cells},
 volume = {10},
 year = {2020}
}