Our researchers in the UK have found vital clues about how melanoma cells become resistant to immunotherapy and how to stop this happening. They hope these findings will bring us closer to a new cure for patients who have advanced melanoma, and have few other treatment options.
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Dr Adam Hurlstone and his team at the University of Manchester in the UK want to improve a type of immunotherapy called an ‘immune checkpoint inhibitor’.
This type of treatment works by taking the brakes off our immune system, helping it to detect and clear cancer. It often works well against melanoma at first. But over time, the treatment can stop working.
Sadly, for 1 in 4 melanoma patients treated with immune checkpoint inhibitors, their cancer will come back within 2 years.
Thanks in part to earlier work by Dr Hurlstone and his team, we already know that melanoma cells can use a molecule called PARP14 to help protect themselves from the action of immune checkpoint inhibitors.
We also know that blocking PARP14 alongside immune checkpoint inhibitors can produce a ‘double whammy’ attack against melanoma cells in the lab - and that this is initially very effective. But, the melanoma cells soon find a way to work around these treatments.
Finding out how melanoma cells do this will unlock new possibilities for more effective cures, and take a potentially brand-new treatment closer to patients.
Curestarter funding has allowed Dr Hurlstone and his team to investigate in detail how this treatment combination can target melanoma cells, by studying mice with melanoma, and also melanoma cells grown in the lab.
Excitingly, the team saw that this treatment combination was very effective in helping our immune system become primed for targeting cancer cells.
The team also investigated how the melanoma cells eventually found other ways to evade this system. They gathered clues suggesting that these two treatments could actually push cancer cells towards using other parts of the immune system to escape.
This new evidence suggests this approach could potentially be effective against melanoma. And thanks to these extra clues, they also know where to look next to help prevent resistance developing. These clues can now be used to help Dr Hurlstone and other researchers further improve immunotherapy treatments for melanoma.
What could this mean for patients in the future?
Drugs which block PARP14 have not yet reached trials in cancer patients, but they have entered early safety studies for people with a different condition. If these trials go well, Dr Hurlstone believes this could be a useful stepping stone towards trialing PARP14 blockers as a new cancer cure.
Dr Hurlstone’s team have found genetic ‘signals’ in melanoma cells which suggest that PARP14 blockers could be particularly effective for certain patients.
This means that one day this could allow doctors to give more ‘personalised’ treatments for patients, and help to make sure that patients receive the most effective treatments for their cancer, as soon as possible.
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