ESTRO 36 Abstract Book

S536 ESTRO 36 _______________________________________________________________________________________________

rectum and bladder. Six blood samples were collected from each patient; pre-treatment, 1 hour (h) post implant, 4h, 24h, 4weeks (w) and at 3 months (m). DNA double strand breaks were stained using the γH2AX and 53BP1 proteins. Patient self-scored quality of life from the Expanded Prostate Cancer Index Composite (EPIC) were obtained at baseline , 1 m, 3m, 6m, 9m, 1 year (y), 2y and 3y post treatment. Spearman’s correlation coefficients were used to evaluate correlations between temporal changes in γH2AX, dose and toxicity Results The minimum follow-up was 2 years. Population mean prostate D 90% was 144.6±12.1 Gy. Rectal near maximum dose D0.1cc = 153.0±30.8 Gy and D2cc= 62.7±12.1 Gy and bladder D0.1cc = 123.1±27.0 Gy and D2cc = 70.9±11.9 Gy. Pre-treatment, mean (±SD) background foci (co-localising γH2AX and 53BP1) was 0.42±0.20 foci per cell (Figure 1B). A Shapiro-Wilk test confirmed the data was normally distributed (w=0.943, p=0.540). Post seed implantation, γH2AX/53BP1 foci numbers were significantly elevated as early as 1 hour post implantation and remained so at 4 and 24 hours, 4 weeks and 3 months post implantation (Figure 1B). The γH2AX/53BP1 foci numbers continued to rise at 4 weeks (672 h) even after reduction in seeds activity due to natural decay (Figure 2A) before dropping at 3 months. EPIC summary scores for bowel, urinary, and sexual domains are presented in Figure 2. Changes in EPIC scores from baseline showed high positive correlation between acute toxicity and late toxicity for both urinary and bowel symptoms. Increased production of γH2AX at 24h relative to baseline positively correlated with late bowel symptoms, EPIC 1y (r= 0.67, p = 0.035), EPIC 2 y (r=0.86, p = 0.001). Overall, no correlations were observed between dose metrics (prostate global or sector doses) and γH2AX foci counts.

Conclusion Our results show that a prompt increase in γH2AX foci at 24 hours post-implant relative to baseline may be a useful measure to assess elevated risk of late RT related toxicities for PPB patients. A subsequent investigation recruiting a larger cohort of patients is warranted to verify our findings.

Poster: Radiobiology track: Radiobiology of breast cancer

PO-0971 Estimating second malignancy risk in IMRT and VMAT in radiotherapy for carcinoma of left breast J. Selvaraj 1 , V. Sakthivel 2 1 The Canberra Hospital, Medical Physics and Radiation Engineering, Canberra, Australia 2 Advanced Medical Physics, Medical Physics, Houston- Texas, USA Purpose or Objective IMRT and VMAT produce dose distributions with superior target dose uniformity and normal tissue sparing. However, this increases amount of volume receiving very low doses substantially compared to conventional techniques. This increases the risk of radiation-induced second malignancy (SCR) as reported in the literature. The aim of this study is to use a mechanistic radiobiological model which is more accurate in predicting the dose- response at low as well as high dose levels to estimate SCR. Studies have shown patient age at exposure is important in estimating SCR, thus patients’ age is also accounted for in the SCR estimation. Moreover, the mechanistic model also takes cell proliferation and dose fractionation into account. Material and Methods Fifty IMRT and VMAT plans with similar dose-volume objectives were selected for the study. The prescription