ESTRO 2020 Abstract book

S375 ESTRO 2020

Mean perturbation, 1mm threshold percentage and mean percentage volume change were calculated per structure. Pointwise mean and SD of distance from raw contours were calculated and t-tests were carried out with a null hypothesis of 0mm edits. Qualitative visual analysis of rendered structures, displaying statistics on a reference surface highlighted systematic edits, occupying areas with large distance magnitude and low SD, and clusters of p -values < 0.01, suggesting that most clinicians made similar edits. Areas with high SD on rendered images may indicate interobserver variability. Results The spinal cord received the most editing (12.55 ± 6.04 mm) due to large superior-inferior displacements at the extremes; the cerebellum received the least (0.64 ± 0.44 mm) – measured by mean perturbation (Table 1). Excluding tubular structures, all structures received a mean perturbation of < 2.8 mm editing. However, summary statistics provide no information on the location of edits needed to more precisely identify systematic changes. Figure 1 shows localised information on renderings of the oral cavity and left parotid. Areas of systematic edits can be observed on the anterior-superior surface of the oral cavity (Figures 1a, 1b & 1c) and the extension of the parotid lobe (Figures 1d, 1e & 1f). Other areas of systematic edits were observed but are not displayed for reasons of space.

Conclusion Edits to DLC contours are generally small, but exhibit variability, with volumetric differences which may lead to DVH and treatment plan variability. Nevertheless, systematic editing, apparent for some clinical DLC contours, may help to identify regions where DLC can be retrained, further reducing human intervention in the segmentation process. Future work will focus on automated methods to decrease clinical variability in editing, using this data to inform the training of future models and predicting the clinical editing of auto contours.

Plenary Session: Highlights of Proffered papers (late- breaking abstracts)

OC-0609 The PET-boost trial: isotoxic homogeneous or FDG-directed dose escalation in stage II-III NSCLC S. Cooke 1 , D. De Ruysscher 2 , B. Reymen 2 , M. Lambrecht 3 , G. Fredberg Persson 4 , C. Faivre-Finn 5 , E. Dieleman 6 , R. Lewensohn 7 , J. Van Diessen 1 , K. Sikorska 8 , F. Lalezari 9 , J. Sonke 1 , J. Belderbos 1 1 netherlands Cancer Institute, Department Of Radiation Oncology, Amsterdam, The Netherlands ; 2 maastricht University Medical Centre, Department Of Radiation Oncology Maastro Clinic- Grow – School For Oncology And Developmental Biology, Maastricht, The Netherlands ; 3 ku Leuven – University Of Leuven, Department Of Oncology- Experimental Radiation Oncology, Leuven, Belgium ; 4 rigshospitalet - University Of Copenhagen, Department Of Oncology, Copenhagen, Denmark ; 5 the Christie Nhs Foundation Trust - University Of Manchester, Department Of Clinical Oncology, Manchester, United Kingdom ; 6 amsterdam Umc - University Of Amsterdam, Department Of Radiation Oncology, Amsterdam, The Netherlands ; 7 karolinska Institute, Department Of Radiation Oncology, Stockholm, Sweden ; 8 netherlands Cancer Institute, Department Of Biometrics, Amsterdam, The Netherlands ; 9 netherlands Cancer Institute, Department Of Radiology, Amsterdam, The Netherlands Purpose or Objective The randomized phase II PET-boost trial(NCT01024829) aimed to improve freedom from local failure(FFLF) by