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Specimens of polycrystalline zirconium were irradiated with 1 MeV singly charged carbon ions using Pelletron accelerator. The ion doses used were in the range 1013 ions/cm2-1015 ions/cm2. The pristine specimen had preferred orientation for (002) and (004) crystallographic planes, which remained unaffected on irradiation with carbon ions. The crystallite size and lattice strain initially increased on irradiation with carbon ion dose 1013 ions/cm2 and later on decreased monotonically with further increase in ion dose till 1015 ions/cm2. Lattice strain increased linearly with the crystallite size. FESEM micrographs showed that carbon ion irradiation on the smooth surface of pristine zirconium specimens produced surface defects in the form of pits, cavities, agglomers and protruded structures of height ≈ 26 µm, which modified the surface properties, such as surface roughness, surface hardness and corrosion resistance. The surface roughness increased substantially on irradiation with carbon ions till 1014 ions/cm2 and later on decreased a little bit from the peak value. The surface hardness followed the classical Hall–Petch relation. The corrosion resistance is significantly improved on irradiation with carbon ions; greater the ion dose better is the corrosion resistance. [ABSTRACT FROM AUTHOR]

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Although promising new radiation therapy techniques such as hadrontherapy are currently being evaluated in the treatment of head and neck malignancies, local control of head and neck squamous cell carcinoma (HNSCC) remains low. Here, we investigated the involvement of cancer stem-like cells (CSCs) in a radioresistant HNSCC cell line (SQ20B). Stem-like cells SQ20B/SidePopulation(SP)/CD44/ALDH were more resistant to both photon and carbon ion irradiation compared with non-CSCs. This was confirmed by a BrdU labeling experiment, which suggests that CSCs were able to proliferate and to induce tumorigenicity after irradiation. SQ20B/SP/CD44/ALDH were capable of an extended G2/M arrest phase in response to photon or carbon ion irradiation compared with non-CSCs. Moreover, our data strongly suggest that resistance of CSCs may result from an imbalance between exacerbated self-renewal and proliferative capacities and the decrease in apoptotic cell death triggering. In order to modulate these processes, two targeted pharmacological strategies were tested. Firstly, UCN-01, a checkpoint kinase (Chk1) inhibitor, induced the relapse of G2/M arrest and radiosensitization of SQ20B-CSCs. Secondly, all-trans retinoic acid (ATRA) resulted in an inhibition of ALDH activity, and induction of the differentiation and radiosensitization of SQ20B/SP/CD44/ALDH cells. The combination of ATRA and UCN-01 treatments with irradiation drastically decreased the surviving fraction at 2Gy of SQ20B-CSCs from 0.85 to 0.38 after photon irradiation, and from 0.45 to 0.21 in response to carbon ions. Taken together, our results suggest that the combination of UCN-01 and ATRA represent a promising pharmacological-targeted strategy that significantly sensitizes CSCs to photon or carbon ion radiation. [ABSTRACT FROM AUTHOR]