A "double whammy" of chemo and immunotherapy could knock out deadly breast cancer, with scientists saying it could provide long-lasting immune protection.

Pairing chemo and immunotherapy can deliver a double-whammy punch that knocks out deadly drug-resistant breast cancer, new research has shown.

Scientists who tested the approach on mice found that animals remained cancer-free even after they were given new tumours, indicating long-lasting immune protection.

Unlike some other cancers, including those of the lung and skin, breast cancer is not known to respond well to treatments that harness the immune system.

But a remarkable transformation was seen when an international team of scientists combined targeted chemotherapy with antibody-based immunotherapy.

Tumours lost their ability to shield themselves from the immune system, allowing immune cells to attack the cancer.

Writing in the journal Science Translational Medicine, researchers led by Dr Philipp Muller, from the University of Basel in Switzerland, described the results as "striking".

An extremely treatment-resistant cancer had been transformed into tumours that were "highly vulnerable to immune attack".

The scientists added: "Ultimately, this resulted in complete cures in our pre-clinical model."

The "target" 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.

Patients with this disease are genetically programmed to over-produce the cancer-driving Her2 protein.

In most cases, patients develop resistance to Her2 targeted treatments such as the drug Herceptin.

The new research involved combining a cancer-destroying chemotherapy drug with certain antibodies, including those that prevent cancer escaping detection by the immune system.

This resulted in immune cells, such as cancer-fighting T-cells, converging on the tumours.

Surprisingly, it also attracted "regulatory T-cells" whose normal job is to tone down immune responses. Removing the regulatory T-cells resulted in the mice developing severe autoimmune disease, demonstrating their crucial role in preventing "collateral damage" during immunotherapy.