A new study has solved a decades-old mystery about why cancer cells respond differently to radiation therapy, a discovery that could lead to more effective cancer treatments. The research, published January 13 in Nature Cell Biology, reveals that DNA repair mechanisms play a surprising role in determining how cancer cells die after radiation exposure.
“The surprising result of our research is that DNA repair, which normally protects healthy cells, determines how cancer cells die following radiotherapy,” said Professor Tony Cesare of Children’s Medical Research Institute (CMRI), who led the study.
Two Different Paths to Cell Death
The researchers discovered that cancer cells can die in two distinct ways after radiation treatment, with vastly different implications for treatment effectiveness. Which path a cell takes depends on how it attempts to repair radiation-damaged DNA.
When cells use a repair method called homologous recombination, they tend to die during cell division – a process that goes unnoticed by the immune system. However, when cells use alternative repair methods, they release substances that alert the immune system, potentially triggering a broader attack against the cancer.
Breakthrough Through Technology
The research team made their discovery by using advanced microscope technology that allowed them to track individual cancer cells for a week after radiation treatment. This long-term observation revealed patterns that had been impossible to detect with previous methods.
The findings also shed new light on why certain breast cancers with mutations in the BRCA2 gene respond differently to radiation therapy. These cells lack the ability to perform homologous recombination, which the study showed affects their death pattern after treatment.
Implications for Treatment
Associate Professor Harriet Gee, a radiation oncologist from Western Sydney Local Health District’s Radiation Oncology Network and co-project lead, noted that these findings answer questions that have puzzled doctors for three decades.
The discovery could lead to new treatment strategies. By blocking homologous recombination with drugs, doctors might be able to force cancer cells to die in ways that activate the immune system, potentially making treatments more effective.
A Team Effort
The research represents six years of work led by Dr. Radoslaw Szmyd, the study’s first author. The project involved collaboration between researchers at CMRI, the Cleveland Clinic in the United States, and the University of Sydney.
The findings are particularly significant because they connect two critical aspects of cancer treatment – radiation therapy and the immune system – in a way that was previously unknown. This understanding could help develop more effective combination therapies that harness both approaches.