Applied radiation and isotopes : including data, instrumentation and methods for use in agriculture, industry and medicine · 2025
Radiobiological effects of AB-BNCT on tongue squamous cell carcinoma: An in vitro and in vivo study.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Huang Hefa, Quan Rui, Zhou Wenming, Wang Haixi, Wu Menglin, Wang Shirui, Chen Weiqiang, Zhuang Ruirong, Guan Xingcai, Zhang Shixu, Mao Aihong, Gu Long, Dai Zhongying, Zhang Lu
Аннотация
This study systematically investigated the radiobiological effects of an accelerator-based boron neutron capture therapy (AB-BNCT) system on SAS cells, a human tongue squamous cell carcinoma (TSCC) cell line. In vitro experimental results showed that L-10B-BPA incubation within 12 h had no significant effect on cell viability. At 24 and 48 h post-irradiation, the 26N20 group exhibited 11 % and 31.91 % reductions in cell viability, accompanied by 82.15 % and 68.34 % decreases in proliferation rates, respectively, compared to controls. In the 26N10 group, 48-h post-irradiation analysis revealed 49.05 % G2/M phase cell cycle arrest and a 40.17 % apoptosis rate (p < 0.05). In vivo experiments revealed that 1 h after L-10B-BPA administration, the boron concentration in tumor tissue reached 59.36 ppm with tumor-to-normal tissue (T/N) ratio reached a maximum value of 8.48. Thirteen days after treatment, a complete tumor response was observed in 33 % of cases, while the objective response rate reached 100 %. Median survival time was significantly prolonged to 68 days from 27days for control (p < 0.05). Notably, at advantage depth, the L-10B-BPA combined with neutron irradiation failed to confer survival benefit. Neutron irradiation alone demonstrated tumor growth-promoting effects at identical fluence levels. These findings underscore the critical need to address dose cold spots in deep-seated tumors during clinical applications. These results indicate that the AB-BNCT system effectively suppresses the progression of TSCC, likely through the induction of DNA damage and apoptosis. Further studies will explore the underlying molecular mechanisms of BNCT-induced apoptosis, providing a scientific basis for its precise clinical application.