S226
ESTRO 36 2017
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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