ICR and Oxford Researchers Find Potential Route to Boost Radiotherapy Response

Image credit: Sangharsh Lohakare on Unsplash (modified)

(IN BRIEF) Scientists at The Institute of Cancer Research, London, and the University of Oxford have uncovered a mechanism that helps cancer cells survive radiotherapy by repairing radiation-induced DNA damage. The study found that insulin-like growth factor 1 receptor, or IGF-1R, helps recruit the DNA repair protein DNA-PKcs to damaged chromatin, enabling cancer cells to repair double-strand breaks through the end-joining process. When IGF-1R is lost or blocked, this repair mechanism becomes defective, leaving cancer cells more vulnerable to radiation. The findings, published in Molecular Oncology and funded by Cancer Research UK, the Medical Research Council and Prostate Cancer UK, reveal a new link between growth signalling and DNA repair machinery. In the longer term, the research could support combination treatment strategies that pair radiotherapy with drugs designed to weaken tumour DNA repair, with potential relevance for prostate cancer and other treatment-resistant cancers.

(PRESS RELEASE) LONDON, 19-Jun-2026 — /EuropaWire/ — Scientists at The Institute of Cancer Research, London, and the University of Oxford have identified a mechanism that helps cancer cells survive radiotherapy, pointing to a potential new route for making radiation treatment more effective.

The study found that insulin-like growth factor 1 receptor, known as IGF-1R, plays an important role in helping cancer cells repair DNA damage caused by radiotherapy. IGF-1R has long been associated with cell growth and survival, but the new research suggests it also acts as part of the cellular machinery that enables cancer cells to respond to treatment-induced damage.

Radiotherapy works by damaging the DNA of cancer cells. One of the most serious forms of damage is a double-strand break, where both strands of the DNA helix are cut. If cancer cells cannot repair these breaks, they are more likely to die. However, many tumours are able to activate repair mechanisms that allow them to survive treatment.

The researchers found that when IGF-1R is lost or blocked, cancer cells become less able to repair double-strand breaks. The study showed that IGF-1R helps recruit DNA-dependent protein kinase catalytic subunit, or DNA-PKcs, to damaged chromatin, the tightly packed structure that organises DNA inside cells.

DNA-PKcs is a key component of non-homologous end joining, one of the main DNA repair processes used by cells to fix double-strand breaks. When IGF-1R is absent, DNA-PKcs is not properly recruited to the damaged area, weakening the repair process and making cancer cells more vulnerable to radiotherapy.

The findings reveal a previously unrecognised link between growth signalling and DNA repair. While IGF-1R has traditionally been studied for its role in cancer growth and survival signalling, the new work suggests it also helps protect tumour cells from the damage caused by radiation.

The research was led by scientists at The Institute of Cancer Research, London, and the University of Oxford, and was published in Molecular Oncology. Funding was provided by Cancer Research UK, the Medical Research Council and Prostate Cancer UK.

In the longer term, the findings could inform new treatment strategies that combine radiotherapy with drugs designed to weaken cancer cells’ ability to repair DNA. By attacking both the tumour and its repair systems, such combinations could potentially improve outcomes for patients with cancers that are difficult to treat.

There is particular interest in the possible relevance of the discovery for prostate cancer, where radiotherapy is commonly used. Researchers believe a subset of patients may benefit from therapies that exploit this newly identified vulnerability, although further work is needed to determine which patients and tumour types would be most suitable.

Before the findings can be translated into clinical practice, scientists will need to validate the results in more complex models that better reflect real tumours. They will also need to identify which cancers rely most heavily on IGF-1R for DNA repair and whether existing or future IGF-1R-targeting drugs can be used safely and effectively in combination with radiotherapy.

The research may also have broader implications beyond prostate cancer. Tumours that become resistant to other DNA repair-targeting treatments could potentially be vulnerable to strategies that interfere with IGF-1R-dependent repair pathways.

Professor Wojciech Niedzwiedz, Group Leader of the Cancer and Genome Instability Group at The Institute of Cancer Research and corresponding author of the study, said the discovery changes how IGF-1R is viewed. He said the receptor has previously been seen mainly as a driver of cancer growth, but the new findings suggest it also functions as part of a cellular defence mechanism against treatment.

Dr Matthew Ellis, first author of the study and now a Research Associate in the Balmus Laboratory at the University of Cambridge, said IGF-1R was already known to be linked to cancer cell survival and treatment resistance, but its effect on the cell’s ability to withstand radiation-induced DNA damage was particularly clear.

He said the hope is that insights into hidden support systems used by cancer cells could eventually lead to more precise and effective treatments, helping radiotherapy become more powerful against resistant tumours.

The study is dedicated to the memory of Dr Valentine Macaulay, whose career included work at The Institute of Cancer Research and focused on improving outcomes for prostate cancer patients through pioneering research on IGF-1R.

Media Contact:

Tel: 0203 437 3502
email: mediaoffice@icr.ac.uk

SOURCE: The Institute of Cancer Research