A breakthrough discovery by Australian researchers has revealed that beta blockers, a cheap blood pressure medication taken by millions worldwide, could help protect women against one of the most aggressive forms of breast cancer by “switching off” a gene that drives tumour progression.
Scientists at Monash University in Melbourne have identified how beta blockers may halt the spread of triple negative breast cancer (TNBC), offering new hope for treating a disease that affects around 8,400 women annually in the UK and has significantly poorer survival rates than other breast cancers.
The research, published in Science Signaling, pinpoints a molecular mechanism involving a gene called HOXC12 that could explain why patients taking beta blockers show improved survival rates. The discovery opens the door to a potential low-cost treatment for a cancer type that has frustrated oncologists due to its limited therapeutic options.
Professor Michelle Halls, senior author and drug discovery expert at Monash Institute of Pharmaceutical Sciences, said the findings confirmed the potential link between beta blockers and reduced tumour progression. “Our colleagues previously found that beta blockers are associated with a significant reduction in mortality in people with triple negative breast cancer,” she said. “Now we have a much better grasp on why this could be the case.”
The research reveals that stress hormones such as cortisol and adrenaline can activate a receptor called beta-2 adrenoceptor, which accelerates cancer spread when triggered. Beta blockers work by dampening these stress hormones’ effects, and the team discovered they can switch off the HOXC12 gene that drives this deadly process.
Triple negative breast cancer accounts for approximately 15 per cent of all breast cancers in the UK and US, affecting around 8,400 British women each year. Unlike other breast cancers, TNBC cells lack receptors for oestrogen and progesterone and don’t overexpress the HER2 protein, making hormone therapies and targeted treatments ineffective.
The aggressive nature of TNBC means it typically grows and spreads faster than other breast cancer types. While 85 per cent of women with breast cancer overall survive for more than five years, the figure drops to just 77 per cent for triple negative cases. In advanced stages where the cancer has spread to distant organs, survival plummets to a devastating 12 per cent.
Mr Terrance Lam, a pharmaceutical PhD candidate and study co-author, emphasised the significance of identifying HOXC12 as a biomarker. “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,” he said.
The Melbourne team’s work builds on a 2023 clinical trial that first established the connection between beta blockers and improved TNBC outcomes, though the underlying mechanism remained unclear until now. Their research examined how two signalling molecules, cAMP and calcium, interact to accelerate cancer spread when the beta-2 adrenoceptor is activated.
Crucially, the study found that patients with high levels of HOXC12 expression had poorer overall survival outcomes, suggesting this gene could serve as a marker to identify which patients would benefit most from beta blocker therapy at the point of diagnosis.
“Triple negative breast cancer is an aggressive cancer which can be especially challenging to treat and identifying new treatment pathways are important,” Lam added, noting the urgent need for alternative therapeutic approaches.
The researchers are now calling for further studies to determine whether HOXC12 can be used as a diagnostic tool to identify patients who would benefit from beta blocker therapy. This personalised approach could help clinicians make more informed treatment decisions and potentially prevent cancer spread in vulnerable patients.
Beta blockers, commonly prescribed for high blood pressure and heart conditions, work primarily by slowing the heart rate and blocking the action of stress hormones. Medications such as propranolol and atenolol are already taken by millions of people worldwide and have well-established safety profiles.
The potential repurposing of these inexpensive drugs for cancer treatment represents a significant opportunity, particularly given the limited options currently available for TNBC patients. Standard treatment typically involves aggressive chemotherapy, surgery, and radiation therapy, but the lack of targeted therapies makes treatment particularly challenging.
Previous research has shown that stress and its associated hormones can accelerate cancer progression. The Melbourne team’s findings provide a biological explanation for this phenomenon and suggest that managing stress responses through medication could play a crucial role in cancer treatment.
The discovery is particularly relevant given that TNBC disproportionately affects younger women and those with BRCA1 gene mutations. Non-Hispanic Black women are twice as likely to develop TNBC compared to other ethnic groups, with 21 per cent of breast cancers in this population being triple negative.
Professor Halls stressed the excitement within the research community about these findings. The team’s previous work had shown that combining beta blockers with anthracycline chemotherapy could enhance treatment effectiveness by preventing nerve growth in tumours, which helps cancer cells spread.
The research also highlights the complex relationship between the nervous system and cancer progression. When anthracycline chemotherapy is administered alone, it can increase sympathetic nerve fibre activity in tumours, potentially aiding cancer spread. Beta blockers appear to counteract this effect.
With approximately 56,000 women diagnosed with breast cancer annually in the UK, the potential impact of this discovery is substantial. The researchers emphasise that while the findings are promising, patients should not start taking beta blockers without medical supervision, as these medications require careful monitoring and dosing.
The next phase of research will focus on clinical trials to validate whether HOXC12 testing at diagnosis can effectively identify patients who would benefit from beta blocker therapy. If successful, this could lead to a paradigm shift in how triple negative breast cancer is treated, offering hope to thousands of women facing this aggressive disease.
As the scientific community continues to explore drug repurposing opportunities, the Melbourne team’s discovery demonstrates how existing medications can offer unexpected benefits in the fight against cancer, potentially transforming outcomes for patients with limited treatment options.
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Image Credit (Shortened):
X-ray of ultrasound‑guided marking of breast cancer – author/license not specified on Commons; use with proper credit if metadata becomes available, via Wikimedia Commons.
