Endorectal contact radiation boosting: making the case for dose and volume reporting.
OC-0633
Abstract
Endorectal contact radiation boosting: making the case for dose and volume reporting.
Authors: Evert Van Limbergen1, Colien Hazelaar1, Femke Vaassen1, Murillo Bellezzo1, An-Sofie Verrijssen2, Yves Willems1, Ben Vanneste1, Gabriel Paiva Fonseca1, Jeroen Buijsen1, Jeroen Leijtens3, Ane Appelt4, Frank Verhaegen1, Maaike Berbee1
1MAASTRO clinic, Department of Radiation Oncology, GROW School for Oncology and Developmental Biology, Maastricht University Medical Centre+ , Maastricht, The Netherlands; 2Catharina Ziekenhuis Eindhoven, Radiation-Oncology, Eindhoven, The Netherlands; 3Laurentiusziekenhuis, Abdominale heelkunde , Roermond, The Netherlands; 4University of Leeds, Institute of Medical Research at St James's, Leeds, United Kingdom
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Purpose or Objective
The various rectal endoluminal brachytherapy techniques
all have steep, but different, depth dose gradients, resulting in very
inhomogeneous dose delivery. In rectal Contact X-ray Therapy (CXT) doses are typically
prescribed and reported to the applicator surface and not to the GTV, CTV and OARs,
the latter of which are crucial to understand tumor response and toxicity rates.
To quantify this problem, we performed a dose
modeling study using a fixed prescription dose to the surface of the applicator
and varying tumor response scenarios (fig 1).
Results
A fixed prescribed dose to the surface of the applicator resulted in a
broad range of cumulative doses delivered to the GTV, CTV and healthy
intestinal wall. Depending on the tumor response scenario the equivalent dose
in fractions of 2 Gy (EQD2) (α/β 10) received by 90%
of the GTV varied between 63 (thick tumor, no response) and 231 Gy (thin tumor,
good response). The highest D2cc of the normal bowel wall was seen in the thin
tumors showing good response and concentric shrinkage (EQD2 D2cc 165 Gy), and
the lowest was seen in thick tumors without shrinkage (EQD2 D2cc 96.5 Gy).
Differences in GTV/CTV and bowel wall dose were predominantly determined by
initial tumor thickness and magnitude of tumor thickness regression during
treatment.