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Immunotherapy could avert cancer relapse

Immunotherapy could prevent cancer cells that survive treatment from using the body’s own immune system to ‘wake up’ and regrow, a study shows.

Immunotherapy could prevent cancer cells that survive treatment from using the body’s own immune system to ‘wake up’ and regrow, a study shows

immune
Programmed death-ligand 1 (PD-L1) protein, which is thought to suppress the immune system.
Blockers of PD-L1 and PD-1 interaction are an important anticancer drug class.
Picture: Science Photo Library 

Immunotherapy could prevent cancer cells that survive treatment from using the body’s own immune system to ‘wake up’ and regrow, a study shows.

Scientists from the Institute of Cancer Research in London worked with colleagues in Leeds, Surrey and the US to examine why cells that have lain dormant for long periods can suddenly turn deadly.

The experiment involved studying the cells of the immune system of mice.

Immune cells normally release signals called TNF-alpha that trigger inflammation in response to trauma or infection, which were found to kill cancer cells.

50%

of people diagnosed with cancer in England and Wales survive for ten years or longer.

Source: Cancer Research UK

However, the team also found these same signals could be hijacked by dormant cancer cells to drive aggressive growth during a relapse.

Immunotherapy aimed at these signals was found to slow or even prevent regrowth by targeting a molecule called PD-L1.

Study co-author Alan Melcher said: ‘Our study finds the body’s own immune system seems to play a crucial role when cancer relapses.

‘The immune system goes from keeping cancer cells in check to awakening and feeding residual cells, while turning a blind eye to their growth.

‘Excitingly, many of the methods employed by treatment-resistant tumours to regrow and hide from the immune system can be blocked using existing immunotherapies.’


Melcher A (et al) (2017) Subversion of NK Cell and TNF-alpha Immune Surveillance Drives Tumor Recurrence. Cancer Immunology Research doi:10.1158/2326-6066.CIR-17-0175

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