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Boron neutron capture therapy (BNCT) is an advanced radiation therapy technique that is rapidly developing in the field of cancer treatment. This technique, an atomic-level binary targeted therapy, kills cancer cells by causing a 10B(n, α)7Li nuclear reaction within the cancer cells, and its clinical implementation requires professional technology and device support. The core elements of BNCT include appropriate neutron sources and neutron capture drugs. Compared with traditional radiotherapy techniques, BNCT shows outstanding advantages in treating locally recurrent tumors, such as central nervous system tumors and head and neck tumors. Furthermore, it can better protect normal organs, especially for tumors that have already significantly invaded surrounding organs, demonstrating its promising future prospects. This article mainly elaborates on the technical principles, core elements, and clinical applications of BNCT, in hope of providing reference for clinical diagnosis and treatment.

Boron neutron capture therapy (BNCT) as a binary targeted particle radiotherapy strategy has shown potent anti‐cancer potential. However, biological barriers and restricted blood supply pose challenges in achieving adequate boron concentration within deep‐seated tumor lesions. BNCT with other anti‐cancer therapies, such as X‐ray radiotherapy and photothermal therapy, is devised to address the limitations of BNCT efficiency. However, the potential risk of organ‐accumulating toxicity and treatment complexity of dual exogenous activation hinders its development. To address this problem, newly redox‐responsive boron nano‐chains (RBNC) are reported that combine BNCT and endogenous chemodynamic therapy (CDT)‐enhanced ferroptosis. RBNC specifically activates nanoparticle size conversion (large‐to‐small) in response to GSH/H2O2 in the tumor microenvironment, releasing boron delivery agents boron quantum dots (BQD) and Fe3+. RBNC exhibits negligible systemic toxicity while demonstrating high boron accumulation at tumor. Meanwhile, the introduction of Fe3+ not only produces ·OH through reaction with H2O2, but also depletes GSH and reduces GPX4 activity in tumors, resulting in amplified intracellular oxidative stress and chemodynamically enhanced ferroptosis. Thus, the work provides a strategy to solve the problem of insufficient boron concentration and poor targeting of boron delivery agents and fill the gaps of BNCT combined with CDT and ferroptosis. [ABSTRACT FROM AUTHOR]

Plasma is highly efficient in the inactivation of microorganisms and is tried to be applied to the treatment of wounds. The gas activated by plasma, named plasma-activated gas, can also effectively inactivate microorganisms and get rid of the limitations of direct plasma treatment. However, the details of the interaction of plasma-activated gas on the tissue are still unclear. In this study, the agarose gel models in the presence of microorganisms to simulate the infected tissues were used to study the inactivation effects and mechanisms of plasma-activated gas. The inactivation depths in the gel models in the presence of microorganisms were related to the types of plasma-activated gas and the species of microorganisms. The Mixed-gas exhibited the strongest inactivation effects, and the inactivation depths in the gel models in the presence of bacteria were deeper than those in the presence of fungi. The long-lived species in the plasma-activated gas penetrated to more than 5.2 mm while the short-lived species only penetrated less than 2.3 mm, demonstrating the distinct roles of reactive species in the inactivation process. Moreover, the pig muscle was covered on the gel models to assess the penetration depths of the plasma-activated gas in muscle tissue and the focused plasma-activated gas could penetrate 1–1.5 mm of pig muscle. This study explored the inactivation effects and mechanisms on the gel models and the penetration depths in the real tissues of plasma-activated gas, which supplied the theoretical basis for the further application of plasma-activated gas in biomedical fields. [ABSTRACT FROM AUTHOR]

Boron neutron capture therapy (BNCT) is an advanced binary tumor‐cell‐selected heavy‐particle radiotherapy used for treating invasive malignant tumors. However, its clinical applications have been impeded by the rapid metabolism and insufficient tumor‐specific accumulation of boron agents. To tackle this issue, we develop a smart boron nanosensitizer (BATBN) capable of transforming its size in response to cancer biomarker for optimal balance between penetration and retention of boron‐10 for BNCT. BATBN comprises an ultrasmall boron quantum dots (BQD) core (4 nm) conjugated with cell‐penetrating peptides, which facilitates its cellular uptake and deep tumor penetration. In the tumor microenvironment, the tumor biomarker can specifically initiate a self‐condensation reaction of BATBN, leading to the formation of larger‐sized nanoaggregates. Due to such a specific intratumoral transformation, BATBN demonstrates a 2.4‐fold increase in intratumoral boron concentration and a 5.0‐fold increase in tumor retention time compared to the BQDs. Thus, the tumor volume of the BATBNs‐treatment group is 2.7‐fold smaller than that of BQDs in preclinical tumor models after 21 days of neutron irradiation treatment. This study presents a supramolecular strategy to endow BNCT agents with the biomarker‐activated size interconversion, permitting precise and efficient BNCT for cancer treatment. [ABSTRACT FROM AUTHOR]

Trifluoroborate boronophenylalanine (BBPA) is a boron amino acid analog of 4‐boronophenylalanine (BPA) but with a trifluoroborate group (−BF3−) instead of a carboxyl group (−COOH). Clinical studies have shown that 18F−labeled BBPA ([18F]BBPA) can produce high‐contrast tumor images in positron emission tomography (PET). Beyond PET imaging, BBPA is a theranostic agent for boron neutron capture therapy (BNCT). Because BBPA possesses an identical chemical structure to BNCT and PET, it can potentially predict the boron concentration for BNCT using [18F]BBPA‐PET. The synthesis of BBPA was achieved by selectively fluorinating the α‐aminoborate compound, taking advantage of the varying rates of solvolysis of the B−F bond. The study showcased the high‐contrast [18F]BBPA‐PET imaging in various tumor models, highlighting its broad applicability for both [18F]BBPA‐PET and BBPA‐BNCT. [18F]BBPA‐PET tumor uptake remains consistent across various doses, including those used in BNCT. This enables accurate estimation of the boron concentration in tumors using [18F]BBPA‐PET. With its dual boron structure, BBPA increases boron concentration in tumor cells and tumor tissues compared to BPA. Thus, less boron carrier is needed. This study introduces a new theranostic boron carrier that enhances boron accumulation in tumors, predicts boron concentration, and enhances the accuracy and effectiveness of BNCT. [ABSTRACT FROM AUTHOR]