Conventional contrast-enhanced MR imaging is the current standard technique for the diagnosis and treatment evaluation of gliomas and other brain neoplasms. However, this method is quite limited in its ability to characterize the complex biology of gliomas and so there is a need to develop more quantitative imaging methods. Perfusion and permeability MR imaging are two such techniques that have shown promise in this regard. This review will highlight the underlying principles, applications, and pitfalls of these evolving advanced MRI methods.

While technological advances in radiation oncology have led to a more precise delivery of radiation dose and a decreased risk of side effects, there is still a need to better understand the mechanisms underlying DNA damage response (DDR) at the DNA and cytogenetic levels, and to overcome tumor resistance. To maintain genomic stability, cells have developed sophisticated signaling pathways enabling cell cycle arrest to facilitate DNA repair via the DDR-related kinases and their downstream targets, so that DNA damage or DNA replication stress induced by genotoxic therapies can be resolved. ATM, ATR, and Chk1 kinases are key mediators in DDR activation and crucial factors in treatment resistance. It is of importance, therefore, as an alternative to the conventional clonogenic assay, to establish a cytogenetic assay enabling reliable and time-efficient results in evaluating the potency of DDR inhibitors for radiosensitization. Toward this goal, the present study aims at the development and optimization of a chromosomal radiosensitivity assay using the DDR and G2-checkpoint inhibitors as a novel modification compared to the classical G2-assay. Also, it aims at investigating the strengths of this assay for rapid radiosensitivity assessments in cultured cells, and potentially, in tumor cells obtained from biopsies. Specifically, exponentially growing RPE and 82-6 hTERT human cells are irradiated during the G2/M-phase transition in the presence or absence of Caffeine, VE-821, and UCN-1 inhibitors of ATM/ATR, ATR, and Chk1, respectively, and the induced chromatid breaks are used to evaluate cell radiosensitivity and their potency for radiosensitization. The increased yield of chromatid breaks in the presence of DDR inhibitors, which underpins radiosensitization, is similar to that observed in cells from highly radiosensitive AT-patients, and is considered here as 100% radiosensitive internal control. The results highlight the potential of our modified G2-assay using VE-821 to evaluate cell radiosensitivity, the efficacy of DDR inhibitors in radiosensitization, and reinforce the concept that ATM, ATR, and Chk1 represent attractive anticancer drug targets in radiation oncology.

The volume of cardiac diagnostic procedures involving the use of ionizing radiation has increased rapidly in recent years, and the radiation exposure experienced by patients undergoing any medical imaging procedure has recently obtained a growing attention. Transradial (TR) access is being increasingly used worldwide for diagnostic coronary angiography (CA), and percutaneous coronary interventions, since it offers several benefits as compared to transfemoral (TF) access, such as by reducing hemostasis time and vascular complications, increased patient comfort, reduced hospital stay, and lower cost. In contrast, TR CA is thought to be associated with increased radiation exposure parameters compared with the traditional TF access. Although experienced operators may almost counterbalance this shortcoming, the increase in radiation exposure associated with TR approach seems not to be present in most clinical settings.