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S226

ESTRO 36 2017

_______________________________________________________________________________________________

provide valuable diagnostic, prognostic or predictive

information for oncological diseases. This information

aims at improving individual patients’ outcomes by a

better treatment selection.

SP-0431 Radiomics in radiotherapy. How is it used to

personalise treatment and to predict toxicity and/or

tumour control

C. Gani

1

1

University Hospital Tübingen Eberhard Karls University

Tübingen, Radiation Oncology Department, Tübingen,

Germany

Radiomics is defined as the automated or semi-automated

extraction of a large number of features from imaging

datasets resulting an individual “imaging phenotype”.

These features and the imaging phenotype can then be

correlated with a variety of other parameters: from

genetic phenotypes to oncological outcome data.

Radiomics as a non-invasive procedure is of particular

interest for the radiation oncologist in times of precision

radiation oncology: The radiomics phenotype might help

to identify patients at high risk for treatment failure and

therefore candidates for more aggressive treatment.

Furthermore radiomics can also be a helpful tool to

predict the risk for radiation-induced toxicities and guide

the dose distribution within normal tissues. This lecture

will give an overview about the existing data on radiomics

in the field of radiation oncology.

SP-0432 Uncertainties in imaging -how they should be

reported and propagated in prediction models using

radiomics

L. Muren

1

Aarhus University Hospital - Aarhus University, Medical

Physics, Aarhus, Denmark

Abstract not received

SP-0433 Imaging biobanks: challenges and

opportunities

A. Van der Lugt

1

1

Erasmus MC University Medical Center Rotterdam,

Department of Radiology, Rotterdam, The Netherlands

An imaging biobank can be defined as an organised

database of medical images and associated imaging

biomarkers (radiology and beyond) shared among multiple

researchers, and linked to other biorepositories. An

imaging biobank is designed for scientific use. Image data

are systematically analysed visually, manual, or (semi)-

automated with the main aim to extract imaging

biomarkers than can be related to patient characteristics

like medical history, genomic data, and outcome or

disease characteristics like genomic data, biomaterials or

response to treatment. The data storage is structured in a

way that the database can be queried and retrieved based

on available metadata. In order to exploit the available

information interactions with other databases are a

perquisite. General requirements with respect to the data

collection are therefore a database facilitating storage of

image data and metadata, storage of derived image-based

measurements, and storage of associated non-imaging

data, taking into account the need to deal with

longitudinal data, and to cope with multiple file formats.

Finally, automated retrieval is needed for image analysis

pipelines that extract image features for radiomics

signatures or for hypothesis free deep learning algorithms.

Symposium with Proffered Papers: Novel approaches in

prostate tumour control

SP-0434 State of the art in prostate tumour

radiobiology

C. Peitzsch

1,2

1

OncoRay - Center for Radiation Research in Oncology,

University Hospital Carl Gustav Carus- Technische

Universität Dresden, Dresden, Germany

2

Nationales Centrum for Tumor diseases NCT- Dresden,

German Cancer Center DKFZ- Heidelberg, Dresden,

Germany

Prostate tumorigenesis is a multistep process from

intraepithelial

neoplasia

(PIN)

and

localized

adenocarcinoma, to castration-resistant prostate cancer

(CRPC) and further into an invasive and metastatic disease

stage with poor prognosis. Several driver and passenger

mutations e.g. within the androgen receptor (

AR

),

ETS

,

TP53

,

PTEN

,

BRCA1/2, CTNNB1

or

ATM

were identified, so

far, to be involved in this developmental process. Beside

this specific genetic features of prostate cancer cells,

cellular heterogeneity within prostate cancer describes

the observation that malignant cells differ within their

phenotypic features and functional properties. This tumor

heterogeneity and cellular plasticity of tumor cells are the

main driving forces for tumor growth, metastasis and

therapy resistance and can be explained by the cancer

stem cell (CSC) hypothesis in combination with clonal

evolution and epigenetic regulation. CSC-specific

molecular mechanisms of radioresistance mainly based on

increased DNA repair capacity, enhanced reactive oxygen

species (ROS) scavenging and induced epithelial-

mesenchymal transition (EMT) and is regulated e.g. by the

androgen-receptor

signaling,

the

tumor

microenvironment, growth factors and cytokines. Data

from our own group indicating that ionizing radiation

themself is modulating epigenetic mechanisms in prostate

cancer cells and thereby cellular plasticity. To translate

these basic research findings into clinically relevant data

primary model systems and mouse models can be used for

pre-clinical validation of radiosensitizer and biomarker

discovery.

SP-0435 Novel developments in molecular targeting of

prostate cancer

R. Bristow

1

1

Princess Margaret Cancer Centre University Health

Network, Radiation Oncology - Room 5-964, Toronto,

Canada

Prostate cancer (CaP) remains the most common male

malignancy worldwide. Although some localized cancers

can be indolent, others can manifest aggressive biology

with abnormal cancer metabolism and genetic instability.

These men need intensified treatment to prevent

metastatic castrate-resistant disease (mCRPC). Recent

studies have started to define the genomic landscape of

prostatic cancer heterogeneity in which mCRPC is

associated with increasing androgen receptor aberrations,

DNA repair deficiencies, mutations in PI3K and tumour

suppressor gene pathways, aberrant WNT-beta-catenin

signaling and defects in cell cycle control. For localized

disease amenable to radiotherapy,we have previously

shown that genetic instability and hypoxia are strong

prognostic factors for prostate cancer outcome.

Subsequently, we have gone on to analyze the whole-

genomes and methylomes of 194 men and the exomes of

479 men to discover multimodal genetic signatures for

responders and non-responders following precision

radiotherapy and surgery. We observed that intermediate

risk prostate cancers have a paucity of clinically-

actionable mutations; in distinct contrast to that reported

for mCRPC. However, all patients with an DDR-associated

ATM mutation failed therapy. A significant proportion of

tumours harbour recurrent non-coding aberrations,

important genomic rearrangements, and a novel

mechanism of PTEN inactivation whereby a local inversion