## 1 Introduction  
Inasmuch as cancer incidence is growing globally, external beam radiotherapy (RT) remains one of most effective strategies in oncological disease management and cure. Recent years have witnessed remarkable technological advances in RT that have improved the precision of the dose distribution to deep-seated tumors [1]. A clear example is prototherapy, whose physical properties ensure greater sparing of healthy tissue than photon-based conventional radiotherapy (CRT), thus abating the risk of RT-induced secondary cancers [2]--a crucial requirement, especially for pediatric patients [3]. However, this is of little avail against tumor radioresistance. Proton beams used clinically are radiobiologically equivalent to photons, with a slightly higher relative biological effectiveness (RBE) equal only to some 10%. Aside from high-RBE carbon ion radiotherapy (CIRT), which is still hampered by costs and a lack of robust evidence-based clinical advantages [4], recently proposed physics-based strategies such as Proton-Boron Capture Therapy (PBCT) have been shown to enhance in vitro proton biological effectiveness [5; 6]. However, PBCT conceptually stems from the much longer standing Boron-Neutron Capture Therapy (BNCT) approach, which is based on the well-known nuclear reaction \({}^{10}\)B(n,\(\alpha\))\({}^{7}\)Li. The rationale of BNCT is that low-energy (0.0025 eV) thermal neutrons interact with \({}^{10}\)B incorporated preferentially by tumor cells, leading to the emission of one \(\alpha\)-particle (\({}^{4}\)He) and one recoiling \({}^{7}\)Li nucleus [7; 8; 9; 10]. As these reaction products have a summed range in the order of a cell nucleus diameter (-10 \(\upmu\)m), in principle, only cancer cells will incur the damage brought about by the emitted particles [11; 12; 13]. Moreover, the high Linear Energy Transfer (LET) possessed by the reaction products is supposed to confer such particles a highly DNA-damaging action. This represents the putative radiobiological cornerstone [14] for the greater effectiveness consistently shown by BNCT both in vitro and in clinical trials. Hence, BNCT may be valuable in overcoming cancer radioresistance [7; 9; 15; 16; 17]. Specifically, [PERSON] et al. recently reviewed the most relevant clinical trials for a variety of disease sites both in terms of boron delivery agents as well as prognosis, spanning from as early as 1951 up to 2019, and reported results that support BNCT is a better overall prospective treatment modality compared to CRT for cancers, such as glioblastoma multiforme, meningiomas, head and neck, lung, sarcomas, melanomas as well as pediatric tumors and metastatic sites, among others [17]. Although radiobiological studies have been carried out [13; 16; 18], the vast majority are understandably on BNCT-induced loss of tumor clonogenicity and cell death in general [19; 20; 21]. Since little has been investigated at the molecular level [20; 22; 23], the actual mechanisms governing the cellular response to BNCT remain to be elucidated. In fact, as recently reviewed in [24], it has been speculated that the BNCT-mixed fields diminish the ability to repair DNA Double-Strand Breaks (DSBs), the most cytotoxic radiation-induced lesion [25; 26], by interfering with DNA Damage Response (DDR) pathways. High-LET radiation predominantly induces clustered DSBs that are associated with a higher lethality due to their poor reparability [26; 27; 28]. As structural chromosome aberrations (CAs) arise from DSB mis-rejoining, a mechanistic link between BNCT-induced cell death and lethal CAs has been long proposed [29] but never substantiated by experimental data. Therefore, in this work, we focused on the measurement of CAs following BNCT as compared to low-LET X-ray irradiations with the specific intent of measuring the level of CA complexity. This is because as the ionization density increases, so does the likelihood that complex-type CAs arise [30; 31; 32], these being defined as involving at least two chromosomes, two arms and three breaks [33].