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内容記述 |
Proton?boron capture therapy (pBCT) has recently attracted attention as a method for enhancing the efficacy of proton therapy. In pBCT, boron-accumulated cancer cells are irradiated with protons to induce the p +11B 3 reaction. The biological efficacy of pBCT has been confirmed by cell-based experiments. However, the actual 3 reaction cross section is relatively small, and the number of particles produced by this reaction is known to be significantly less than that in the primary proton beam. Therefore, the effectiveness of pBCT has not been theoretically elucidated, and its physical origin and biological effects remain controversial. Consequently, in this study, we sought to clarify these mechanisms by verifying their physical and biological aspects. First, we explored the possibility that other -particle production channels as alternatives to the 3 reaction were the cause of the pBCT effect. The results suggested the existence of other -particle production reaction channels, as predicted by theoretical calculations. However, these cross sections were not large enough to support the effectiveness of pBCT. Thus, to investigate the efficacy of pBCT, including biochemical factors that are not limited to -particle production, experiments were performed to measure the cell viability during proton irradiation. The measurements used boronophenylalanine (BPA) and sodium borocaptate (BSH), which are two boron delivery agents used in boron neutron capture therapy (BNCT). However, no significant changes were observed with respect to the conventional proton therapy. Based on these results, the biological efficacy of pBCT remained unconfirmed under our experimental conditions, and the effectiveness of pBCT needs to be carefully discussed in the future. |
