ABSTRACT
Objectives: This study compared plans of high definition (HD), 2.5 mm width multi-leaf collimator (MLC), to standard, 5 mm width, isocentric linear accelerator (linacs), CyberKnife (CK), and Gamma Knife (GK) for stereotactic radiosurgery (SRS) techniques on multiple brain metastases. Methods: Eleven patients undergoing SRS for multiple brain metastases were chosen. Targets and organs at risk (OARs) were delineated and optimized SRS plans were generated and compared. Results: The linacs delivered similar conformity index (CI) values, but the gradient index (GI) for HD MLCs was significantly lower (P-value <.001). Half the OARs received significantly lower dose using HD MLCs. CK delivered a significantly lower CI than HD MLC linac (P-value <.001), but a significantly higher GI (P-value <.001). CI was significantly improved with the HD MLC linac compared to GK (P-value = 4.591 × 10-3), however, GK delivered a significantly lower GI (P-value <.001). OAR dose sparing was similar for the HD MLC TL, CK, and GK. Conclusions: Comparing linacs for SRS, the preferred choice is HD MLCs. Similar results were achieved with the HD MLC linac, CK, or GK, with each delivering significant improvements in different aspects of plan quality. Advances in knowledge: This article is the first to compare HD and standard width MLC linac plans using a combination of single isocentre volumetric modulated arc therapy and multi-isocentric dynamic conformal arc plans as required, which is a more clinically relevant assessment. Furthermore, it compares these plans with CK and GK, assessing the relative merits of each technique.
ABSTRACT
Radon-222 is a naturally occurring radioactive gas that is responsible for approximately half of the human annual background radiation exposure globally. Chronic exposure to radon and its decay products is estimated to be the second leading cause of lung cancer behind smoking, and links to other forms of neoplasms have been postulated. Ionizing radiation emitted during the radioactive decay of radon and its progeny can induce a variety of cytogenetic effects that can be biologically damaging and result in an increased risk of carcinogenesis. Suggested effects produced as a result of alpha particle exposure from radon include mutations, chromosome aberrations, generation of reactive oxygen species, modification of the cell cycle, up or down regulation of cytokines and the increased production of proteins associated with cell-cycle regulation and carcinogenesis. A number of potential biomarkers of exposure, including translocations at codon 249 of TP53 in addition to HPRT mutations, have been suggested although, in conclusion, the evidence for such hotspots is insufficient. There is also substantial evidence of bystander effects, which may provide complications when calculating risk estimates as a result of exposure, particularly at low doses where cellular responses often appear to deviate from the linear, no-threshold hypothesis. At low doses, effects may also be dependent on cellular conditions as opposed to dose. The cellular and molecular carcinogenic effects of radon exposure have been observed to be both numerous and complex and the elevated chronic exposure of man may therefore pose a significant public health risk that may extend beyond the association with lung carcinogenesis.
