SCOTTISH scientists have discovered a new way of triggering the death of cancer cells which they believe could be more effective than methods currently in use.

And Dr Stephen Tait, the man who led the research team at the University of Glasgow, said that while it was too early to call it a breakthrough, he was excited by its potential and the “very promising” results thus far.

The new method is called Caspase-Independent Cell Death (CICD), and it led to the complete eradication of tumours in experimental models.

Most anti-cancer therapies currently in use – chemotherapy, radiation and immunotherapy – kill cancer cells through a process called apoptosis, which activates proteins called caspases, leading to cell death.

However, apoptosis therapies often fail to kill all the cancer cells, which leads to a recurrence of the disease and can also have unwanted side effects that may even promote cancer.

The Glasgow team wanted to develop a way to improve therapies that induce cancer cell death while mitigating unwanted toxicity.

Tait, from the Cancer Research UK Beatson Institute, Institute of Cancer Sciences, said: “Our research found that triggering CICD, but not apoptosis, often led to complete tumour regression.

“Especially under conditions of partial therapeutic response, as our experiments mimic, our data suggests that triggering tumour-specific CICD, rather than apoptosis, may be a more effective way to treat cancer.”

Unlike apoptosis, which is a silent form of cell death, when cancer cells die through CICD they alert the immune system through the release of inflammatory proteins.

The immune system can then attack the remaining tumour cells that have evaded initial therapy-induced death.

“The way in which we’ve killed the cancer cell alerts the immune system, so even if a therapy doesn’t initially kill all the tumour cells, the immune system is activated to kill the remaining cancer,” said Tait.

His team used lab-grown colorectal cancer cells to show the advantage of killing cancer cells this way, but these benefits may also be applicable to a wide range of cancer types.

“In essence, this mechanism has the potential to dramatically improve the effectiveness of anti-cancer therapy and reduce unwanted toxicity,” he said.

“Taking into consideration our findings, we propose that engaging CICD as a means of anti-cancer therapy warrants further investigation.”

Tait said the multi-disciplinary and multinational work would continue to find out if caspase inhibitors already in use for diseases such as heart attack or stroke could have the same effect.

“If that’s the case it could happen very soon – within three to five years I’d imagine we could think about clinical trials with these drugs.

“If it requires us to develop new inhibitors, that’s going to be a much longer-term project – I’d imagine maybe something in the region of five to ten years.

“Beyond being pleased with the work I’m really excited about the potential of it to really have some clinical effects at the end ... the results look very promising so far.”

Dr Justine Alford, Cancer Research UK’s senior science information officer, added: “Although many cancer treatments work by triggering apoptosis, that method sometimes fails to finish the job and instead may lead to the tumour becoming harder to treat.

“This new research suggests there could be a better way to kill cancer cells which, as an added bonus, also activates the immune system.

“Now scientists need to investigate this idea further and, if further studies confirm it is effective, develop ways to trigger this particular route of cell death in humans.”

The paper is published in the journal Nature Cell Biology.