Triple negative breast cancer explained

When someone is diagnosed with triple negative breast cancer, it means their cancer cells don’t have 3 molecules called receptors commonly seen in other breast cancers.

These receptors are for the hormones oestrogen and progesterone and a third protein called Human Epidermal Growth Factor Receptor 2 (HER2).

More than 8,000 women are diagnosed with triple negative breast cancer in the UK each year. That’s around 15% of breast cancer diagnoses. Currently, we have limited targeted treatments options available for triple negative breast cancer. That’s because hormone therapies and HER2-targeted drugs don’t work on these tumours.

So, our scientists are working tirelessly to understand more about this type of breast cancer and find new ways to treat it. And they’re making headway already.

Professors Andrew Tutt and Chris Lord found a new weakness linked to a gene called HORMAD-1. This gene is usually active in reproductive cells, but it’s also switched on in many triple negative breast cancers.

HORMAD1 can cause mistakes and damage to build up when cancer cells divide. Our researchers found that blocking other proteins these cells rely on could push this damage too far and slow tumour growth. It’s an early but promising route towards a targeted treatment.

Professor Ester Hammond and her team also revealed another weakness we can target. They found that a protein called TPM3 plays a key role in how cancer cells adapt to low oxygen environments in and around triple negative breast cancers.

When they blocked TPM3 from working as it usually would, the triple negative breast cancer cells were less able to spread. And, when combined with chemotherapy treatments it made these drugs more effective.

With fewer targeted treatments available, improving existing ways to treat triple negative breast cancer is important too. 

Immune checkpoint blockade (ICB) is a type of immunotherapy already used to treat thousands of people living with this type of breast cancer. But sometimes, tumours can find ways to resist it.  

Professor Pascal Meier and his team found that changing how cancer cells die can act like an alarm signal that wakes up the immune system and boosts treatment response. 

They showed that in mice, neither immunotherapy nor a drug called tolinapant stopped tumour growth on their own alone. But when combined, 45% of tumours responded. Adding a third drug increased this to 71%, and some tumours disappeared completely.

It’s still early research. But it could lead to stronger, longer-lasting immunotherapy combinations.

And when treatment isn’t working, every cycle matters. Professors Andrew Tutt and Sheeba Irshad investigated whether PET scans could show how someone’s cancer is responding after just 1 cycle of chemotherapy.

In a small study, changes seen on these early scans were strongly linked to whether the cancer had a complete response by the end of treatment. The scans also predicted the response better than standard MRI scans taken partway through treatment.

This research could help doctors spot sooner when chemotherapy isn’t working. Allowing healthcare teams to adjust treatment or explore other options before valuable time is lost. 

We’re making incredible progress in triple negative breast cancer research, but there’s still so much to be done. Treatments don’t work for everyone. And when the disease spreads, it can’t currently be cured.

Through our research, we’re revealing how cancer escapes treatment. Finding its hidden weaknesses. Developing new drugs. And finding smarter ways to get the right treatment to each person sooner.