Correlation of LET with MRI changes in brain and potential implications for normal tissue complication probability for meningioma patients treated with pencil beam scanning proton therapy.

Abstract

PURPOSE\nTo investigate the correlation between imaging changes in brain normal tissue and the spatial distribution of linear energy transfer (LET) for a cohort of meningioma patients treated with scanned proton beams. Then, assuming imaging changes are induced by cell lethality, to study the correlation between normal tissue complication probability and LET.\n\n\nMETHODS\nMRI T2/FLAIR acquired at different intervals after proton radiation were co-registered with the planning CT images from 26 patients diagnosed with meningioma with abnormalities after proton radiotherapy. For this purpose, the T2/FLAIR areas not on the original MRIs were contoured and LET values for each voxel in the patient geometry were calculated to investigate the correlation between the position of imaging changes and LET at those positions. To separate the effect of dose as inductor of these changes, we compared LET in these areas with a sample of voxels matching the dose distributions across the image change areas. Patients with higher LET in image change areas were grouped to verify whether they shared common characteristics.\n\n\nRESULTS\n11 of the patients showed higher LETd in imaging change regions than in group of voxels with the same dose. This group of patients had significantly shallower targets for their treatment than the other 15 and used fewer beams and angles.\n\n\nCONCLUSION\nThis study points towards the possibility of areas with imaging change are more likely to occur in regions with high dose or in those areas with lower dose but increased LETd. The effect of LETd on imaging changes seems to be more relevant when treating superficial lesions with few non opposed beams. However, most of the patients did not show spatial correlation between their image changes and the LETd values, limiting the cases for the possible role of high LET as a toxicity inductor.