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S526

ESTRO 36 2017

_______________________________________________________________________________________________

the use of predictive biomarkers for assessing

radiotherapy related toxicity.

Poster: Radiobiology track: Radiobiology of proton and

heavy ions

PO-0960 Radiobiological effectiveness and its role in

modelling secondary cancer risk for proton therapy

A. Madkhali

1,2

, C. Timlin

1

, M. Partridge

1

1

University of Oxford, Oncology, Oxford, United Kingdom

2

King Saud University, Medicine, Riyadh, Saudi Arabia

Purpose or Objective

In proton therapy, a radiobiological effectiveness ratio

(RBE) of 1.1 (RBE

1.1

) is often used. In reality, RBE depends

on dose, linear energy transfer (LET), biological end point,

and tissue type. Using a value of RBE that may be not

accurate may affect dose calculation and hence,

outcome.

Material and Methods

We used an in-house built code for modelling malignant

induction probability (MIP) from voxel-by-voxel dose map

(Timlin 2014) and implement a published model to

calculate structure-specific RBE, recalculate dose and

MIP, and compare the outcomes with initial calculations

using RBE

1.1

. MIP was calculated using linear quadratic

(LQ), linear (LIN), and linear-no-threshold (LNT) models

for proton therapy plans for an adult and a teenage

patient diagnosed with medulloblastoma (MB). The MIP

was then re-calculated using the RBE model by Dale and

Jones which is a function of dose (d), α and β and RBE

min

and

RBE

max:

Results

Results are shown in Table 1. The difference in MIP by

using RBE

1.1

and RBE

MinMax

is ~2-3%. The effect on mean

dose varies between different organs and is between 6%

and 8%. Clinical implications due to difference in RBE

depend on beam characteristics, dose, structures

concerned, and the volume irradiated.

Conclusion

Using RBE

1.1

makes proton therapy dose and dose-

dependent predictions less accurate. Our results using a

RBE calculation model show that decreased accuracy may

have clinical implications, which agrees with published

literature (Jones 2012; Jones, 2014), and may affect

secondary cancer risk and normal tissue complication

probability calculations as well.

PO-0961 DNA damage and repair influence tumor

sensitivity to diffusing alpha emitters radiation therapy

Y. Keisari

1

, R. Etzyoni

1

, H. Bittan

2

, E. Lazarov

2

, M. Efrati

1

,

M. Schmidt

2

, T. Cooks

1

, L. Arazi

2

, I. Kelson

2

1

Tel-Aviv University / Faculty of Medicine, Clinical

Microbiology and Immunology, Tel-Aviv, Israel

2

Tel Aviv University, School of Physics and Astronomy-

Sackler Faculty of Exact sciences, Tel Aviv, Israel

Purpose or Objective

We developed an alpha radiation based brachytherapy,

which provides efficient ablation of solid tumors by alpha

radiation. This treatment termed,

Diffusing Alpha

emitters Radiation Therapy

(DaRT) utilizes radium-224

loaded wires, which when inserted into the tumor release

by recoil short-lived alpha-emitting atoms. These atoms

disperse in the tumor, and spray it with highly destructive

alpha radiation.

DaRT achieved substantial tumor growth retardation,

extended survival, and reduced lung metastases in mice

bearing various mouse and human derived tumors. Better

tumor control was achieved when DaRT was applied with

chemotherapy. Furthermore, tumor ablation by DaRT

boosted anti-tumor immune responses.