ESTRO 2020 Abstract book

S421 ESTRO 2020

sensitivity at the ventricular wall and a significantly increased RBE. The model coefficients produce a linear RBE model that compares well to published preclinical RBE models. Our model offers the potential to reduce patient risk by avoiding the observed risk hot spots, combined with an accurate patient risk prediction. This affords biological treatment planning based on clinical data. OC-0689 Shrinking-field concept spares the periventricular region in proton therapy of gliomas J. Eulitz 1 , C. Hahn 1 , F. Raschke 2 , C. Karpowitz 3 , W. Enghardt 4 , E. Troost 2 , M. Krause 3 , A. Lühr 1 1 Oncoray - National Center for Radiation Research in Oncology, Medical RadiationPhysics, Dresden, Germany ; 2 Oncoray - National Center for Radiation Research in Oncology, Image-Guided High-Precision Radiotherapy, Dresden, Germany ; 3 Oncoray - National Center for Radiation Research in Oncology, Translational Radiooncology and Clinical Radiotherapy, Dresden, Germany ; 4 Oncoray - National Center for Radiation Research in Oncology, Medical Radiation Physics, Dresden, Germany Purpose or Objective Recent findings suggest an increased radiosensitivity of the cerebral periventricular region in primary brain tumor patients (PVR; Eulitz 2019, Harrabi 2019). Since treatment-associated brain injury correlates with elevated dose and linear energy transfer (LET) (Peeler 2016), the potential of shrinking-field concepts (SFC) in dose and LET sparing of the PVR needs to be assessed. We compared observed radiation-induced brain injuries after proton therapy for glioma patients treated either with uniform dose (UD) or with SFC, and introduce an approach for dedicated PVR-adapted proton treatment planning. Material and Methods All grade II and III glioma patients treated between 2014 and 2018 with (adjuvant) proton radio(chemo)therapy to a total dose ( D ) of 54-60 Gy(RBE) were considered for analysis. 33% of the patients received SFC (with sequential- or simultaneously-integrated boost (SIB)) with a prescribed dose reduction of 6-10 Gy(RBE) in the outer part of the target volume. Contrast enhancements (CE) on follow-up MRI (fuMRI) diagnosed as treatment-related brain injury lesions (symptomatic or clinically silent) were traced back to the fuMRI of first appearance, delineated and deformably co-registered to the planning CT. The distance between CE lesions to the cerebral ventricles was determined. The PVR was estimated as a 4 mm band around the segmented cerebral ventricles. D and LET within the CE lesions were simulated and the PVR volume V X% receiving more than X% of prescribed dose was derived. Brain injury-free survival (in/outside PVR) was derived in a Kaplan-Meyer analysis. For a SIB patient with a CE lesion 10 months after proton therapy, PVR-sparing treatment planning was performed. Results For the SFC and UD patient cohort, the observed CE lesions clustered in direct proximity to the cerebral ventricles with median distances of 2.6 mm and 2.3 mm, respectively. Mean dose at the CE lesion was 54.4±3.5 Gy(RBE) and 56.4±4.3 Gy(RBE) and the corresponding LET value 2.7±0.4 keV/µm and 3.2±0.9 keV/µm, respectively. The SFC reducedV 100% and V 90% in the PVR by 11.3% and 35.3%, respectively. No significant difference was found in one-year symptomatic ( p = 0.15) and asymptomatic ( p = 0.75) injury free survival. An average CE lesion dose of 55 Gy(RBE) was derived within PVR tissue for all patients and

used as PVR tolerance dose. Incorporating the PVR as an organ at risk in treatment plan optimization reduced the V 55Gy(RBE) within the CE lesion and PVR contour by 19.1% and 2.0%, respectively, without compromising target coverage, plan robustness or clinical dose constrains (Fig. 1).

Conclusion For both treatment concepts, late brain injury showed a remarkably similar proximity to the cerebral ventricles and dependence on D and LET. The SFC spares parts of the PVR from high dose and has the potential to improve treatment outcome. However, significant reduction of brain toxicity may require a dedicated PVR dose sparing planning strategy minimizing V 55Gy(RBE) . OC-0690 Dose-dependent changes in subcortical deep grey matter structures after cranial radiotherapy S. Nagtegaal 1 , S. David 2 , M. Philippens 1 , A. Leemans 2 , J. Verhoeff 1 1 UMC Utrecht, Radiation Oncology, Utrecht, The Netherlands ; 2 UMC Utrecht, Image Sciences Institute, Utrecht, The Netherlands Purpose or Objective Irradiation of healthy brain tissue can lead to anatomical and functional deficits, a phenomenon known as radiation- induced brain injury. Especially cognitive and executional impairments can lead to a marked decrease in the patient’s quality of life after radiation therapy (RT), and have been linked to morphological changes in the brain. Of particular interest have been white matter, hippocampus and cerebral cortex. Less is known about the effects of RT the subcortical grey matter (GM) structures. Atrophy of deep GM structures is associated with impaired cognitive function in patients with multiple sclerosis, Alzheimer’s disease, and dementia, suggesting these structures are involved in cognitive processes. Therefore, the relation between deep GM volume and RT dose needs to be examined, to help elucidate the cause of post-RT cognitive decline. Material and Methods We selected 31 patients with high quality follow-up scans who were treated with RT for glioma (grade II-IV) in our institution. The CAT12 (Computational Anatomy Toolbox)