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Metal‐based nanoparticles applied to potentiating the effects of radiotherapy have drawn significant attention from the research community and are now available clinically. By improving our mechanistic understanding, nanoparticles are likely to evolve to provide very significant improvements in radiotherapy outcomes with only incremental increase in cost. This review critically assesses the inconsistent observations surrounding physical, physicochemical, chemical and biological mechanisms of radiosensitization. In doing so, a number of needs are identified for continuing research and are highlighted. The large degree of variability from one nanoparticle to another emphasizes that it is a mistake to generalize nanoparticle radiosensitizer mechanisms. Nanoparticle formulations should be considered in an analogous way as pharmacological agents and as a broad class of therapeutic agents, needing to be considered with a high degree of individuality with respect to their interactions and ultimate impact on radiobiological response. In the same way that no universal anti‐cancer drug exists, it is unlikely that a single nanoparticle formulation will lead to the best therapeutic outcomes for all cancers. The high degree of complexity and variability in mechanistic action provides notable opportunities for nanoparticle formulations to be optimized for specific indications. This article is categorized under: Therapeutic Approaches and Drug Discovery > Emerging Technologies Nanotechnology Approaches to Biology > Nanoscale Systems in Biology
Metal‐based nanoparticles applied to potentiating the effects of radiotherapy have drawn significant attention from the research community and are now available clinically. By improving our mechanistic understanding, nanoparticles are likely to evolve to provide very significant improvements in radiotherapy outcomes with only incremental increase in cost. This review critically assesses the inconsistent observations surrounding physical, physicochemical, chemical and biological mechanisms of radiosensitization. In doing so, a number of needs are identified for continuing research and are highlighted. The large degree of variability from one nanoparticle to another emphasizes that it is a mistake to generalize nanoparticle radiosensitizer mechanisms. Nanoparticle formulations should be considered in an analogous way as pharmacological agents and as a broad class of therapeutic agents, needing to be considered with a high degree of individuality with respect to their interactions and ultimate impact on radiobiological response. In the same way that no universal anti‐cancer drug exists, it is unlikely that a single nanoparticle formulation will lead to the best therapeutic outcomes for all cancers. The high degree of complexity and variability in mechanistic action provides notable opportunities for nanoparticle formulations to be optimized for specific indications. This article is categorized under: Therapeutic Approaches and Drug Discovery > Emerging Technologies Nanotechnology Approaches to Biology > Nanoscale Systems in Biology
Introduction Radiotherapy is a widely recognized first-line clinical treatment for cancer, but its efficacy may be impeded by the radioresistance of advanced tumors. It is urgent to improve the sensitivity of radioresistant tumors to radiotherapy. In this work, gadolinium oxide nanocrystals (GONs) were utilized as radiosensitizers to enhance the killing effect and reinforce the immune activation of X-ray irradiation on 4T1 breast cancer cells in vitro and in vivo. Methods 1.0 T small animal MR imaging (MRI) system was employed to trace GONs in vivo, while 225 kVp X-ray irradiation equipment was utilized for investigating the radiosensitization of GONs in 4T1 breast cancer cells in vitro and in vivo. Western blot, quantitative real-time PCR (RT-qPCR), immunohistochemistry, immunofluorescence, clonal survival assay, flow cytometry and reactive oxygen species assay were used to explore the biological mechanism of GON sensitization. Results GONs exhibited exceptional utility as contrast agents for both in vivo and in vitro MRI imaging. Interestingly, a single dose of 8.0 Gy X-rays together with GONs failed to confer superior therapeutic effects in tumor-bearing mice, while only 3.0 Gy × 3 fractions X-rays combined with GONs exhibited effective tumor growth inhibition. Moreover, fractionated X-ray irradiation with GONs demonstrated a superior capacity to activate the cGAS-STING pathway. Discussion Fractionated X-ray irradiation in the presence of GONs has demonstrated the most significant activation of the anti-tumor immune response by boosting the cGAS-STING pathway.
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