By Chigbu Nwaobia
Scientists at Monash University in Melbourne say beta blockers – which work by dampening the effects of stress hormones – may also halt the progression of triple-negative breast cancer in some patients.
The link between beta blockers and breast cancer first emerged in 2023, though it was not clear why. Now, researchers believe they have identified the mechanism – and with it a potential low-cost treatment for an extremely aggressive disease.
According to Health Digest, their work looked at the interaction between two signalling molecules, cAMP and calcium, which accelerate cancer spread when a receptor called the beta-2 adrenoceptor is activated.
Stress hormones such as cortisol can trigger this receptor, fuelling tumour growth. But the team has now discovered that beta blockers can switch off a gene – HOXC12 – that drives this process, slowing the progression of the disease.
The researchers said the breakthrough could help doctors identify, at the point of diagnosis, which patients are most likely to benefit from beta blocker therapy.
Beta blockers like atenolol work mainly by blocking the effect of stress hormones like adrenaline to slow down the heart. They are currently used to treat a number of conditions, including heart failure, high blood pressure and sometimes anxiety.
Professor Michelle Halls, senior author of the study and an expert in drug discovery biology at the Monash Institute of Pharmaceutical Sciences, said the findings were exciting, as they confirmed the potential link between beta blockers and tumour progression.
“Our colleagues previously found that beta blockers are associated with a significant reduction in mortality in people with triple-negative breast cancer. Now we have a much better grasp on why this could be the case,” she said.
Mr Terrance Lam, a pharmaceutical PhD candidate at the institute and co-author of the study, added: ‘Our collective research strongly suggests that HOXC12 is a potential new indicator for when triple negative breast cancer patients could respond to beta blocker targeted interventions.