ArticleJapanese journal of radiology2026
Enhancing radiosensitivity of boron neutron capture therapy for liver cancer with homologous recombination repair inhibitor.
Article in Japanese journal of radiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundHepatocellular carcinoma (HCC), particularly in recurrent or treatment-refractory cases, often exhibits poor responsiveness to radiation therapy, increasing the risk of radiation-induced liver disease, necessitating innovative treatment approaches. Boric acid-mediated boron neutron capture therapy (BA-BNCT) has emerged as a promising approach for liver cancer. This study aims to improve BA-BNCT efficacy for radioresistant HCC by exploring sensitization agents, enhancing treatment while minimizing irradiation doses and side effects.
methodsWe targeted the DNA homologous recombination repair (HRR) protein RAD51. Before neutron irradiation, a RAD51 inhibitor, B02, was administered to evaluate its sensitization effect on both HepG2 and the radioresistant HepG2R cells. We examined the cell death mechanism, focusing on the expression profile of LC3B after BA-BNCT, to investigate its impact on DNA repair responses, especially on autophagy and apoptosis.
resultsWe observed that inhibition of RAD51 led to increased γH2AX, the DNA double-strand break marker. Additionally, combining the RAD51 inhibitor B02 with BA-BNCT resulted in tumor cell arrest in the G
conclusionsCombining a RAD51 inhibitor with BA-BNCT significantly enhances the anti-tumor efficacy against radioresistant HCC and parental HCC cells. This proof-of-concept study suggests that the combination treatment can achieve comparable or superior therapeutic effects using lower radiation doses, thereby reinforcing the potential of BNCT for treating recurrent HCC.
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