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PURPOSE: This work aims to simulate clustered DNA damage from ionizing radiation and estimate the relative biological effectiveness (RBE) for radionuclide (rBT)- and electronic (eBT)-based surface brachytherapy through a hybrid Monte Carlo (MC) approach, using realistic models of the sources and applicators. METHODS: Damage from ionizing radiation has been studied using the Monte Carlo Damage Simulation algorithm using as input the primary electron fluence simulated using a state-of-the-art MC code, PENELOPE-2018. Two 192 Ir rBT applicators, Valencia and Leipzig, one 60 Co source with a Freiburg Flap applicator (reference source), and two eBT systems, Esteya and INTRABEAM, have been included in this study implementing full realizations of their geometries as disclosed by the manufacturer. The role played by filtration and tube kilovoltage has also been addressed. RESULTS: For rBT, an RBE value of about 1.01 has been found for the applicators and phantoms considered. In the case of eBT, RBE values for the Esteya system show an almost constant RBE value of about 1.06 for all depths and materials. For INTRABEAM, variations in the range of 1.12-1.06 are reported depending on phantom composition and depth. Modifications in the Esteya system, filtration, and tube kilovoltage give rise to variations in the same range. CONCLUSIONS: Current clinical practice does not incorporate biological effects in surface brachytherapy. Therefore, the same absorbed dose is administered to the patients independently on the particularities of the rBT or eBT system considered. The almost constant RBE values reported for rBT support that assumption regardless of the details of the patient geometry, the presence of a flattening filter in the applicator design, or even significant modifications in the photon energy spectra above 300 keV. That is not the case for eBT, where a clear dependence on the eBT system and the characteristics of the patient geometry are reported. A complete study specific for each eBT system, including detailed applicator characteristics (size, shape, filtering, among others) and common anatomical locations, should be performed before adopting an existing RBE value.

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By using the statistical techniques of the ANOVA means test and regression, it was found that theNKRcalibration factor of Standard Imaging (SI) model HDR 1000 plus chambers presents a quadratic dependence with the Reference air kerma rateKR(from 6.9 mGy h-1to 43.9 mGy h-1). In order to understand and correct this dependency one model is presented for total recombination:ks=I300I150=1+kini+kd+kvol·I300+kscreen·I3002,wherekiniis the initial recombination,kvolthe thermal diffusion recombination,kvolthe volumetric recombination andkscreenthe screening for the currents/charges collected at the potential differences of 300 and 150 V. In conclusion, the total recombinationksis composed by onekiniwith a constant contribution of 0.019%, onekdcontribution of 0.017%, onekvol·I300contribution from 0.022% to 0.138%, and thekscreen·I3002effects from 0.002% to 0.09% in the range ofK̇Rrate above. However, when this model forksis applied to try to correct the quadratic dependence of theNKRversusKR,explicitly there is no improvement in the variation range of 0.5% of theNKRversusKR.Nonetheless, it allows to obtainNKRvalues consistent with auc ≤ 0.7%, which is less than 1.25% reported in the literature by ADCLs or SSDLs.

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PURPOSE: To investigate the effects of high dose rate (HDR) brachytherapy on cellular progression of a radioresistant human squamous cell carcinoma in vitro, based on clinical parameters. MATERIALS AND METHODS: An acrylic platform was designed to attach tissue culture flasks and assure source positioning during irradiation. At exponential phase, A431cells, a human squamous cell carcinoma, were irradiated twice up to 1100 cGy. Cellular proliferation was assessed by Trypan blue exclusion assay and survival fraction was calculated by clonogenic assay. DNA content analysis and cell cycle phases were assessed by flow cytometry and gel electrophoresis, respectively. Cellular death patterns were measured by HOPI double-staining method. RESULTS: Significant decreasing cellular proliferation rate (p < 0.05) as well as reduced survival fraction (p < 0.001) in irradiated cells were observed. Moreover, increased percentage of cells arrested in the G2/M phase (32.3 ± 1.5%) in the irradiated group as compared with untreated cells (8.22 ± 1.2%) was detected. Also, a significant (p < 0.0001) nuclei shrinking in irradiated cells without evidence of necrosis or apoptosis was found. CONCLUSION: HDR brachytherapy led to a decreased proliferation rate and cell survival and also hampered cellular progression to mitosis suggesting that tumor cell death mainly occurred due to mitotic death and G2/M cell cycle arrest.

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