Report on the 17^th International Wolfsberg Meeting on Molecular Radiation Biology/Oncology

Hurdal, Norway, 21-23 June 2025

By Ilaria Colauzzi, travel grant awardee

I took part in the Wolfsberg Meeting for the first time this year. I enjoyed the venue and the strong sense of community that characterises the meeting, arising from dynamic poster sessions and discussions. Moreover, informal activities that were organised at the end of each day allowed for more relaxed interactions. The conference was a full immersion in radiobiology, from fundamental research to clinical applications and novel therapies, which made the meeting highly translational.

Although radiotherapy is widely used in cancer treatment for its efficacy, in a subset of patients, the treatment fails due to intrinsic or acquired radioresistance. It is critical that we understand the mechanisms behind this in order to identify target proteins and improve treatment outcomes. In this context, I was glad to present my poster entitled “Identification of new metabolic and stemness-related proteins responsible for radioresistance in triple-negative breast cancer models” within the intra‑ and inter‑cellular signalling section. It was a great opportunity to receive feedback from fellow researchers and to share ideas about future experiments.

Radioresistance was discussed by other researchers in both lectures and posters. These researchers linked it to various mechanisms, such as radiation-induced senescence, modulation of homologous recombination factor expression, and metabolic reprogramming. As I am also investigating metabolic switching in radioresistant cells, I found the lectures that correlated metabolism and radiation response particularly interesting. Dr. Paola Francica (University of Bern, Switzerland) presented her work on the mitochondrial ECHDC2 gene and DNA damage. She showed that the loss of ECHDC2 in breast cancer cells decreased mitochondrial respiration, and therefore the amount of reactive oxygen species generated and the subsequent DNA damage, with resulting radioresistance.

Professor Daniel Wahl (University of Michigan, USA) showed another mechanism by which metabolism and DNA damage were correlated,  for highly radioresistant glioblastoma (GBM) cells. He showed that cancer cells exhibit a high rate of nucleotide synthesis, which is crucial for effective DNA repair, while healthy brain cells prioritise the tricarboxylic acid cycle and neurotransmitter synthesis. These findings are representative of the implications of metabolic alterations in DNA damage and cell survival.

Radioresistance in GBM was also the topic of the talk by Prof Bipasha Mukherjee (UT Health San Antonio, USA), who presented findings on how senescence can drive radioresistance. Her work shows that irradiated GBM cells senesce rapidly and secrete senescence-associated factors that can activate JAK-STAT3 and the NF-kB pathway in non-senescent GBM cells and increase proliferation. Her team found that by targeting these factors as an adjuvant treatment after radiotherapy, they could induce apoptosis in senescent cells.

Ilaria Colauzzi
Pole of Pharmacology and Therapeutics
Institute of Experimental and Clinical Research
Université Catholique de Louvain
Brussels, Belgium

LinkedIn handle: www.linkedin.com/in/ilaria-colauzzi