Triple negative breast cancer: beta -blockers already known and inexpensive could stop its progression

Triple negative breast cancer: beta -blockers already known and inexpensive could stop its progression
What if a simple medication has been prescribed for decades against hypertension has become an unexpected weapon against one of the most formidable breast cancers? An Australian team has just revealed how beta -blockers could act as a switch to curb the spread of triple negative tumors.

Poorly known to the general public, triple negative breast cancer is one of the most difficult to treat. The discovery of an unprecedented mechanism now opens an unexpected track: to divert simple beta -blockers, inexpensive drugs, to stop the spread of tumor cells.

Betabloquents and triple negative breast cancer

Triple negative breast cancer represents around 15 % of cases and is distinguished by its aggressiveness. It is devoid of hormonal receptors (progesterone and estrogens) as well as the HER2 protein on their cells. Therefore, they cannot benefit from the treatments that target these three markers. Patients therefore have few options, and relapses are frequent.

In recent years, several signals suggested that drugs used against heart disease could have a beneficial effect. A meta-analysis has shown that taking beta-blockers was associated with a 26 % reduction in mortality in women with triple negative breast cancer. Small clinical trials have also indicated that propranolol, administered before surgery, decreased certain markers linked to the spread of tumor cells. But until then, the exact mechanism remained mysterious.

An unprecedented mechanism unveiled by an Australian study

Researchers at Monash University have examined the action of beta-adrenergic receptors in tumor cells in detail. They discovered that one of these receptors, beta2, would trigger a real self-employment loop between two cell messengers-calcium and ampc-which promotes the invasion of cancer cells.

By testing 11 lines of triple negative breast cancer, they observed that in six of them, the activation of this receiver systematically resulted an acceleration of the tumor invasion. By looking for the trigger, they identified the HOXC12 gene, which acts as a switch. When this gene is inactivated, the calcium/ampc loop is broken and the cells lose their invasion capacity.

As Terrance Lam sums up, the main author of the study published in Science signaling : “Our results highlight HOXC12 as a key factor that allows the beta2 receiver to stimulate invasion in triple negative breast cancer “.

A new accessible therapeutic hope

These discoveries strengthen the idea that a already available, inexpensive and well -known medicine of doctors, could become an option to slow down the progression of triple negative breast cancer. Unlike new often expensive targeted treatments, beta -blockers have been prescribed for decades for hypertension or heart disease.

Professor Michelle Halls, from Monash University, underlines the issue of this discovery: “Our research reveals how beta -blockers could be reused to block the spread of triple negative breast cancer“.

The idea of ​​a therapeutic repositioning opens the way to larger clinical trials, with the hope of quickly offering a new strategy to patients, without delay years of pharmaceutical development.