It was shown that radiation effects in tumor cells treated with fast neutrons may be increased by the neutron capture reaction${}^{10}{\rm B}({\rm n},\alpha){}^{7}{\rm Li}$. The classic approach for macroscopic dosimetry in fast-neutron therapy cannot be applied to the dose in boron neutron capture therapy (BNCT). The effectiveness of BNCT in killing tumor cells depends on the number of10 B atoms delivered to the tumor, the subcellular distribution of10 B and the thermal neutron fluence at the site of the tumor. Monte Carlo calculations of the energy depositions of short-range particles with high LET coming from10 B disintegrations were performed and compared to the observed biological effects. The simulation allows us to study the influence of the localization of intracellular10 B in the nucleus, cytoplasm, plasma membrane or extracellular space. The biological response function which describes the probability of the lethal effect produced by a single particle track through the cell nucleus was found by comparing the calculated microscopic dose distribution spectra for single events with the survival observed experimentally. Calculations for a human melanoma cell population treated as a monolayer in the presence or absence of boron with d(14)+Be neutrons will be demonstrated. Two different boron compounds enriched in10 B were investigated in this study: boric acid (${\rm H}_{3}{}^{10}{\rm BO}{}_{3}$) and p-dihydroxyboryl phenylalanine (BPA). The study shows that a high fraction of BPA enters the cytoplasm while boric acid was found only in the extracellular space. The computer simulations indicate that BPA yields a higher potential effectiveness for inactivation of melanoma cells than boric acid.

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