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Journal Articles

Oxygen enhancement ratios of cancer cells after exposure to intensity modulated X-ray fields; DNA damage and cell survival

Matsuya, Yusuke; McMahon, S. J.*; Butterworth, K. T.*; Naijo, Shingo*; Nara, Isshi*; Yachi, Yoshie*; Saga, Ryo*; Ishikawa, Masayori*; Sato, Tatsuhiko; Date, Hiroyuki*; et al.

Physics in Medicine & Biology, 66(7), p.075014_1 - 075014_11, 2021/04

 Times Cited Count:4 Percentile:48.97(Engineering, Biomedical)

Hypoxic cancer cells within solid tumours show radio-resistance, leading to malignant progression in fractionated radiotherapy. When prescribing dose to tumours under heterogeneous oxygen pressure with intensity-modulated radiation fields, intercellular signalling could have an impact on radiosensitivity between in-field and out-of-field cells. However, the impact of hypoxia on radio-sensitivity under modulated radiation intensity remains uncertain. In this study, we investigate the impact of hypoxia on in-field and out-of-field radio-sensitivities using two types of cancer cells. These in vitro measurements indicate that hypoxia apparently impacts out-of-field cells, although the OER values in out-of-field cells were smaller compared to those for in-field and uniformly irradiated cells. These decreased radio-sensitivities of out-of-field cells were shown as a consistent tendency for both DSB and cell death endpoints, suggesting that radiation-induced intercellular communication is of importance in treatment planning with intensity-modulated radiotherapy.

Journal Articles

A Theoretical cell-killing model to evaluate oxygen enhancement ratios at DNA damage and cell survival endpoints in radiation therapy

Matsuya, Yusuke; Sato, Tatsuhiko; Nakamura, Rui*; Naijo, Shingo*; Date, Hiroyuki*

Physics in Medicine & Biology, 65(9), p.095006_1 - 095006_12, 2020/05

 Times Cited Count:5 Percentile:47.72(Engineering, Biomedical)

Radio-resistance induced under low oxygen pressure plays an important role in malignant progression in fractionated radiotherapy. For the general approach to predict cell killing under hypoxia, cell-killing models (e.g., the Linear-Quadratic model) have to be fitted to ${it in vitro}$ experimental survival data for both normoxia and hypoxia to obtain the oxygen enhancement ratio (OER). However, model parameters for every oxygen condition needs to be considered by model-fitting approaches. This is inefficient for fractionated irradiation planning. Here, we present an efficient model for fractionated radiotherapy the integrated microdosimetric-kinetic model including cell-cycle distribution and the OER at DNA double-strand break endpoint. The cell survival curves described by this model can reproduce the ${it in vitro}$ experimental survival data for both acute and chronic low oxygen concentrations. The OER$$_{DSB}$$ used for calculating cell survival agrees well with experimental DSB ratio of normoxia to hypoxia. This work provides biological effective dose (BED) under various oxygen conditions including its uncertainty, which can contribute to creating fractionated regimens for multi-fractionated radiotherapy. If the oxygen concentration in a tumor can be quantified by medical imaging, the present model will make it possible to estimate the cell-killing and BED under hypoxia in more realistic intravital situations.

Journal Articles

Modeling of yield estimation for DNA strand breaks based on Monte Carlo simulations of electron track structure in liquid water

Matsuya, Yusuke; Kai, Takeshi; Yoshii, Yuji*; Yachi, Yoshie*; Naijo, Shingo*; Date, Hiroyuki*; Sato, Tatsuhiko

Journal of Applied Physics, 126(12), p.124701_1 - 124701_8, 2019/09

 Times Cited Count:24 Percentile:81.84(Physics, Applied)

Biological effects after ionizing radiation exposure arise from initial DNA strand breaks. DNA damage can be estimated from the simulation with both track structure analysis and diffusion of free radicals; however, the simulation is a time-consuming process. In this study, we present a simple model for estimating yields of strand breaks based only on spatial patterns of inelastic interactions (i.e., ionization and electronic excitation) generated by electrons, which are evaluated by PHITS code without considering the production and diffusion of free radicals. In this model, the number of events per track and that of the two events pair within 3.4 nm (corresponding to 10 base pair) were stochastically sampled for calculating SSB and DSB yields, respectively. The calculated results agreed well with other simulations and experimental data on DSB yield and yield ratio of DSB/SSB for the exposure to mono-energetic electrons. The present model also can demonstrate the relative biological effectiveness at the DSB endpoint for various photon exposures. This study indicated that the spatial pattern of inelastic events composed of ionization and electronic excitation is sufficient to obtain the impact of electrons on initial induction to DNA strand break.

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