It is now widely accepted that the immune system plays an important role in protecting the body against cancer. Some researchers believe that our immune defences are constantly identifying and killing rogue cells that have mutated into precancerous tumours. So it comes as little surprise that scientists are attempting to use the body’s own immune defences in the fight against cancer.
Perhaps the moment this strategy came of age was in 2013 when cancer immunotherapy was named 'Breakthrough of the Year' by the journal Science. The judges of the breakthrough prize freely admitted that they had some qualms about awarding such an experimental approach with their most coveted accolade, but in the end they had to admit that cancer immunotherapy, although still a long way from becoming routine practice, had, in several important respects, passed muster.
“The field hums with stories of lives extended: the woman with a grapefruit-size tumour in her lung from melanoma, alive and healthy 13 years later; the 6-year-old near death from leukaemia, now in third grade and in remission; the man with metastatic kidney cancer whose disease continued fading away even after treatment stopped,” Science reported. “Immunotherapy marks an entirely different way of treating cancer—by targeting the immune system, not the tumour itself. Oncologists, a grounded-in-reality bunch, say a corner has been turned and we won't be going back.”
Just as the immune system is complex, then so are the many varied forms of cancer immunotherapy. One approach is to genetically modify a patient’s own T-cells to make them target tumour cells. This so-called chimeric antigen receptor (CAR) therapy is a personalised form of cancer treatment. CAR T-cells have produced dramatic improvements when tested in clinical trials – in one early trial more than half of leukaemia patients went into complete remission.
Other approaches have concentrated on lessening the natural inhibition of T-cells – in effect taking the “brakes” off so that the T-cells become potent killers free to destroy rogue cancer cells. This is done by producing targeted antibodies, known as monoclonal antibodies (MABs), that are directed against the “braking” molecules such as CTLA-4 and PD-1 (programmed death), which are known to act at T-cell inhibitors. This is the basis of drugs such as ipilimumab, now a licensed treatment for metastatic melanoma.