ESTRO 36 Abstract Book

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S861 ESTRO 36
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performance status, and total tumor dose. The BN model
has an AUC of 0.67 (95% CI: 0.59–0.75) on the external
validation set and an AUC of 0.65 on a 5-fold cross-
validation on the training data. A model based on TNM
stage performed with an AUC of 0.49 (95% CI: 0.39-0.59)
on the validation set.
Conclusion
The distributed learning model outperformed the TNM
stage based model for predicting 2-year survival in a
cohort of NSCLC patients in an external validation set (AUC
0.67 vs. 0.49). This approach enables learning of
prediction models from multiple hospitals while avoiding
many boundaries associated with sharing data. We believe
that Distributed learning is the future of Big data in health
care.
References
[1] Dehing-Oberije C. et al. Int J Radiat Oncol Biol Phys
2008;70:1039–44. doi:10.1016/j.ijrobp.2007.07.2323.
EP-1597 Focal dose escalation in prostate cancer with
PSMA-PET/CT and MRI: planning study based on
histology
C. Zamboglou1, I. Sachpazidis2, K. Koubar2, V. Drendel3,
M. Werner3, H.C. Rischke1, M. Langer 4, F. Schiller5, T.
Krauss4, R. Wiehle 2, P.T. Meyer5, A.L. Grosu1, D. Baltas2
1 Medical Center - University of Freiburg, Department of
Radiation Oncology, Freiburg, Germany
2 Medical Center - University of Freiburg, Division of
Medical Physics- Department of Radiation Oncology,
Freiburg, Germany
3 Medical Center - University of Freiburg, Department of
Pathology, Freiburg, Germany
4 Medical Center - University of Freiburg, Department of
Radiology, Freiburg, Germany
5 Medical Center - University of Freiburg, Department of
Nuclear Medicine, Freiburg, Germany
Purpose or Objective
First studies could show an increase in sensitivity when
primary prostate cancer (PCa) was detected by addition of
MRI and PSMA PET/CT information. On the other side the
highest specificity was achieved when the intersection
volume between MRI and PSMA PET/CT was considered.
Aim of this study was to demonstrate the technical
feasibility and to evaluate the tumor control probability
(TCP) and normal tissue complication probability (NTCP)
of IMRT dose painting using combined 68Ga-HBED-CC PSMA-
PET/CT and multiparametric MRI (mpMRI) information in
patients with primary PCa.
Material and Methods
7 patients (5 intermediate + 2 high risk) with biopsy-
proven primary PCa underwent 68 Ga-HBED-CC-PSMA
PET/CT and mpMRI followed by prostatectomy. Resected
prostates were scanned by ex-vivo CT in a localizer and
prepared for histopathology. PCa was delineated on
histologic slices and matched to ex-vivo CT to obtain GTV-
histo. Ex-vivo CT including GTV-histo and MRI data were
matched to in-vivo CT(PET). Contours based on MRI (GTV-
MRI, consensus volume by two experienced radiologist),
PSMA PET (GTV-PET, semiautomatic using 30% of SUVmax
within the prostate) or the combination of both (GTV-
union/-intersection) were created. Three IMRT plans were
generated for each patient: PLAN77, which consisted of
whole-prostate radiation therapy to 77 Gy in 2.2 Gy per
fraction; PLAN95, which consisted of whole-prostate RT to
77 Gy in 2.2 Gy per fraction, and a simultaneous
integrated boost to the GTV-union (Plan95union)/-
intersection (Plan95intersection ) to 95 Gy in 2.71 Gy per
fraction. The feasibility of these plans was judged by their
ability to reach prescription doses while adhering to the
FLAME trial protocol. TCPs based on co-registered
histology after prostatectomy (TCP-histo), and normal
tissue complication probabilities (NTCP) for rectum and
bladder were compared between the plans.
Results
All plans for all patients reached prescription doses while
adhering to dose constraints. The average volumes of GTV-
histo, GTV-union and GTV-intersection were 7±8 ml, 9±9
ml and 3±4 ml. In Plan95 union and Plan95intersection the mean
doses on GTV-histo were 95.7±1.5 Gy and 90.7±6.9 Gy,
respectively (p=0.016). Average TCP-histo values were
63±29%, 99±1% and 90±11% for Plan77, Plan95 union and
Plan95 intersection respectively. PLAN95union had significantly
higher TCP-histo values than Plan77 (p=0.016) and
Plan95 intersection (p=0.03). There were no significant
differences in rectal and bladder NTCPs between the 3
plans.
Conclusion
IMRT dose painting for primary PCa using combined 68Ga-
HBED-CC PSMA-PET/CT and mpMRI was technically
feasible. A dose escalation to GTV-union resulted in
significantly higher TCPs without higher NTCPs.
EP-1598 Modelisation of radiation response at various
fractionation from histopathological prostate tumors
V. Aubert1,2, O. Acosta1,2, N. Rioux-Leclercq3, R.
Mathieu4, F. Commandeur1,2, R. De Crevoisier1,2,5
1INSERM, U1099, Rennes, France
2University Rennes 1, LTSI, Rennes, France
3Rennes Hospital and University, Department of
Pathology, Rennes, France
4CHU Pontchaillou, Department of Urology, Rennes,
France
5Centre Eugène Marquis, Department of Radiotherapy,
Rennes, France
Purpose or Objective
Using simulation from histopathological cancer prostate
specimen, the objectives were to identify the total dose
corresponding to various fractionations necessary to
destroy the tumor cells (50% to 99.9%) and to assess the
impact of the Gleason score on these doses.
Material and Methods
Histopatological specimen were extracted from 7 patients
having radical prostatectomy. A senior uropathologist
manually delineated all tumor foci on the hematoxylin and
eosin-stained axial slides and assigned Gleason scores (GS)
to each individual focus. Antibodies CD31 were used as
blood vessel markers. Three slide samples per patient,
corresponding to a surface of 2000µm x1200µm, were
scanned and used within a simulation model developed in
the Netlogo software (Figure 1). The model contained the
following cells: tumor cells with a density ranging from
45% to 85%, endothelial cells with a density ranging from
0.3 to 8% and normal cells. The samples were GS:7 (3+4)
for 47.6%, GS:7 (4+3) for 28.6% and GS:8 (4+4) for 23.8%.
We used the equations of the model simulating the
radiation response of hypoxic tumors published by
Espinoza et al. (Med Phys 2015). The model parameters
were adjusted to biological values from the literature:
diffusion coefficient (2.10-9 m²/s), Vmax and Km of oxygen
consumption (15 and 2.5 mmHg), tumor cells proliferation
(1008 hours), half-life of dead cells (168 hours), α (0.15
Gy-1) and β (0.048 Gy-2) of the linear-quadratic model.
Three fractionations were tested, at 2, 2.5 and 3
Gy/fraction at 24h interval. Five simulations were
performed by slide sample. The objectives were to
identify the total dose, at each fractionation, to kill 50%
to 99.9% of the tumor cells.