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‘Double-whammy’ of chemo and immunotherapy could knock out deadly breast cancer

November 30th, 2015

For a long time the role of the immune system in the control and elimination of cancer has been underappreciated. However, it is now understood that tumours can suppress the anti-tumour immune response in order to aid their own growth and spread around the body.

Unlike some other cancers, including those of the lung and skin, breast cancer doesn’t respond well to treatments that harness the immune system. However, new research has shown that pairing chemo and immunotherapy can deliver a double-whammy punch that knocks out deadly drug-resistant breast cancer.

The new research involved combining a cancer-destroying chemotherapy drug with certain antibodies, including those that prevent cancer escaping detection by the immune system. The results show that the tumours lost their ability to shield themselves from the immune system, allowing immune cells to attack the cancer. The models also remained cancer-free even after they were given new tumours, indicating long-lasting immune protection.

The researchers led by Dr Philipp Muller, from the University of Basel in Switzerland, described the results as “striking” – an extremely treatment-resistant cancer has been transformed into tumours that are highly vulnerable to immune attack, and ultimately resulted in complete cures in their pre-clinical model.

The subtype of breast cancer used in the study was a form known as Her2 positive, which affects between 15 per cent and 20 per cent of women with breast cancer, and can be difficult to treat.

Patients with this disease are genetically programmed to over-produce the cancer-driving Her2 protein and most patients develop resistance to Her2 targeted treatments, such as the drug Herceptin.

NBCF currently funds a researchers doing similar studies; exploring how to trigger the immune system to recognise tumours and eliminate them, by combining drug combinations with chemo or radiation to enhance the effect of the treatments.