Christopher J Tien1, David J Carlson2, Ravinder Nath3, Zhe Jay Chen3. 1. Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, CT. Electronic address: chtien@gmail.com. 2. Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, CT; Department of Radiation Oncology, University of Pennsylvania Perelman Center for Advanced Medicine, Philadelphia, PA. 3. Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, CT.
Abstract
PURPOSE: This work quantifies the influence of intrafraction DNA damage repair and cellular repopulation on biologically effective dose (BED) in Ir-192 high-dose-rate brachytherapy for prostate cancer. In addition, it examines the effect of source-decay-induced BED variation for patients treated at different time points in a source exchange cycle. MATERIALS AND METHODS: Current fractionation schemes are based on simplified-form BED = nd(1 + d/(α/β)), which assumes that intrafraction repair, interfraction repair, and repopulation are negligible. We took accepted radiobiological parameters of Tk, Tp, and α from the recommendations of the AAPM TG-137, and recalculated the full-form BED. Fraction times were normalized to require 15 min for 20 Gy at 10 Ci. Calculations were carried out for both α/β = 1.5 and 3 Gy. RESULTS: After accounting for intrafraction repair, interfraction repair, and/or repopulation, full-form BED calculations showed significant values, as compared with simplified-form BED. For 1-fraction 20 Gy fractionation, the full-form BED was only 64-82% of the simplified-form BED. Dose protraction effects were milder for smaller prescriptions (6 Gy/Fx), where full form was 87-94%. With regard to source decay, BED varied >20% for patients treated at the beginning and the end of a source exchange cycle for 20 Gy single-fraction prescription. CONCLUSIONS: Repair and repopulation can be significant in monotherapy high-dose-rate for prostate cancer. As fractionation schemes are established, the simplified BED calculation may not be appropriate. Investigators should consider evaluating BED as a range rather than a discrete value when presenting results unless source activity is explicitly incorporated as well.
PURPOSE: This work quantifies the influence of intrafraction DNA damage repair and cellular repopulation on biologically effective dose (BED) in Ir-192 high-dose-rate brachytherapy for prostate cancer. In addition, it examines the effect of source-decay-induced BED variation for patients treated at different time points in a source exchange cycle. MATERIALS AND METHODS: Current fractionation schemes are based on simplified-form BED = nd(1 + d/(α/β)), which assumes that intrafraction repair, interfraction repair, and repopulation are negligible. We took accepted radiobiological parameters of Tk, Tp, and α from the recommendations of the AAPM TG-137, and recalculated the full-form BED. Fraction times were normalized to require 15 min for 20 Gy at 10 Ci. Calculations were carried out for both α/β = 1.5 and 3 Gy. RESULTS: After accounting for intrafraction repair, interfraction repair, and/or repopulation, full-form BED calculations showed significant values, as compared with simplified-form BED. For 1-fraction 20 Gy fractionation, the full-form BED was only 64-82% of the simplified-form BED. Dose protraction effects were milder for smaller prescriptions (6 Gy/Fx), where full form was 87-94%. With regard to source decay, BED varied >20% for patients treated at the beginning and the end of a source exchange cycle for 20 Gy single-fraction prescription. CONCLUSIONS: Repair and repopulation can be significant in monotherapy high-dose-rate for prostate cancer. As fractionation schemes are established, the simplified BED calculation may not be appropriate. Investigators should consider evaluating BED as a range rather than a discrete value when presenting results unless source activity is explicitly incorporated as well.