Dr
Peter van Luijk
(Dept. of Radiation Oncology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands)
17/10/2012, 10:00
Normal Tissue Damage
oral (invited speaker)
The risk of early radiation pneumonitis limits the radiation dose and efficacy of radiotherapy of thoracic tumours. Besides lung dose, in rats (1) and patients (2) dose to the heart was shown to be a risk factor of radiation pneumonitis. Here we investigated whether the enhanced damage caused by combined heart and lung irradiation can be understood from their individual effects on...
Prof.
Uwe Schneider
(University of Zurich and Radiotherapy Hirslanden)
17/10/2012, 11:00
Normal Tissue Damage
oral (invited speaker)
In developed countries, more than half of all cancer patients receive radiotherapy at some stage in the management of their disease. A radiation-induced secondary malignancy can be the price of success if the primary cancer is cured. Therefore, there is increasing concern regarding radiation-related second cancer risks in long-term radiotherapy survivors and a corresponding need to be able to...
Dr
Fabien MILLIAT
(Institute for Radiological Protection and Nuclear Safety)
17/10/2012, 11:30
Normal Tissue Damage
oral (15 minutes)
Normal tissue damage after radiation therapy is characterised by a chronic altered phenotype of endothelium. Molecular mechanisms involved in the initiation and the acquisition of a chronic activated phenotype of endothelial cells after radiation exposure remain unclear. The aim of this work is to characterize in vitro molecular actors involved in both the acute and late activated phenotype of...
Ms
Lindsay Beaton
(Health Canada)
17/10/2012, 11:50
Normal Tissue Damage
oral (15 minutes)
Whole chromosome fluorescence in situ hybridization (FISH) allows for the detection and identification of chromosome translocations in metaphase spreads. Previous research has shown that radiation induced translocations correlate with both acute and late effects after radiotherapy [1]. This study has examined the incidence of translocations, after exposure to in vitro radiation, in both...
Dr
Hargita Hegyesi
(NRIRR "Frédéric Joliot-Curie" National Research Institute for Radiobiology and Radiohygiene)
17/10/2012, 12:10
Normal Tissue Damage
oral (15 minutes)
BACKGROUND AND PURPOSE: Tumor protein 53-induced nuclear protein-1 (TP53INP1) encodes two nuclear protein isoforms (TP53INP1 and TP53INP1) and transcription is activated by p53. Overexpression of TP53INP1 promotes apoptosis and cell cycle arrest in different tumor cell lines. Therefore, TP53INP1 appears as a key element in p53-mediated cell death and cell cycle arrest, induced by cellular...
