Researchers from the University of Dundee have identified a new mechanism that enables an aggressive form of breast cancer to survive and grow, a vital step towards developing life-saving treatments for the disease.
Triple-negative breast cancer is considered to be more aggressive than other subtypes of the disease, with patients experiencing a poorer prognosis, mainly due to a lack of specific therapies. Studies have shown that triple-negative breast cancer, which accounts for 15% of all breast cancer diagnoses, is more likely to spread beyond the breast and more likely to recur after treatment.
A team of researchers from the University’s School of Medicine have discovered that a protein called DYRK2 promotes triple-negative breast cancer tumour progression, and that patients with high levels of DYRK2 have a poorer survival expectancy than those with low levels.
DYRK2 belongs to a type of protein that can be targeted and stopped from working to promote tumour growth using specific compounds called inhibitors. As such, the Dundee study builds on previous research to demonstrate the potential relevance that DYRK2 inhibitors could have in the clinic, opening the door for potential new future treatments.
“Breast cancer is a complex disease grouped into various subtypes, based on their characteristics,” said Dr Laureano de la Vega, who led the research. “We don’t have any medicines specifically designed to attack triple-negative breast cancer, which is more aggressive than most other types of breast cancer, and patients have a poorer outlook as a result.
“Understanding how triple-negative breast cancer tumours grow and why they are so aggressive is key to developing new strategies and treatments to improve patient survival rates. However, if we want to translate our finding to the clinic, it is not enough to identify mechanisms that promote tumour growth. We also need to find ways to stop those mechanisms using medicines.
“By showing that the protein DYRK2 was helping triple-negative breast cancer cells to survive and to be aggressive, and that the levels of DYRK2 impacted on survival expectancy, we have identified a potential novel therapeutic target. The challenge for ourselves and other teams now is to design new medicines that can stop DYRK2 from working, and to test them in humans. It will also be important to develop ways to identify a sub-population of patients that could benefit the most from these medicines.”
The study was funded by Cancer Research UK and carried out in collaboration with colleagues from the University of Glasgow and the University of California San Diego. The research is published in the latest edition of Cell Death & Differentiation. Dr Rita Moreno Dorta is the first author of the paper.