The scientists who developed the compound, from the Howard Hughes Medical Institute (HHMI), have outlined their research in the latest version of the journal Cancer Cell.

It has been known for years that Smac - second mitochondrial activator of caspases - is part of the cell's complex machinery that enables defective or unnecessary cells to commit suicide (apoptosis).

In healthy cells, Smac is kept in the mitochondria but on receiving an apoptotic signal, it is released and triggers programmed cell death. It does this through binding to and suppressing the so called inhibitor of apoptosis proteins (IAP).

Cancer cells, however, can survive Smac's death signal by switching off the apoptotic machinery. The HHMI researchers, led by Xiaodong Wang discovered that small molecule mimetics of Smac can enter the cell and trigger apoptosis, independently of a signal from the mitochondria.

However, there was a problem. When they were testing the drugs in different cancer cell lines, they discovered that it could only kill cancer cells in the presence of a second protein called tumour necrosis factor alpha (TNF alpha).

Happily though, in their latest work Wang and his colleagues discovered that when they tested 50 different non-small-cell lung cancer (NSCLC) cell lines, roughly a quarter of them were sensitive to treatment with the Smac mimetic alone.

When they introduced those sensitive cells into mice and allowed them to produce tumours, Wang found that the potential drug caused the tumours to regress and, in some cases, even disappear.

"These findings made us wonder what it was about these cell lines that made them sensitive to the Smac mimetic alone," said Wang. "Cancer cells are hard to kill, but these cell lines seemed to have already become sensitized to apoptosis."

Further studies revealed that the sensitive cell lines produced their own TNF alpha and were already 'primed' for apoptosis. The paradox, explained Wang, is that TNF alpha signalling also gives cancer cells a survival signal, offering them a growth advantage.

"Thus, in these cancer cell lines, the TNF alpha survival advantage turns out to be a fatal flaw, because the same pathway can be switched to apoptosis by Smac mimetics," he said.

Wang is hopeful that the compound could be used as a single treatment agent in some cancers and pointed out that clinicians could use the presence of TNF alpha to act as a biomarker of which tumours will respond to it.

The researchers also found that some breast cancer and melanoma cell lines were sensitive to the Smac mimetic alone.

"People have been suspecting for a long time that some cancer cells may somehow turn on their apoptotic pathway already," said Wang.

"And now we know what pathway they turn on and why. We can take advantage of this phenomenon for potential cancer therapy by switching a signal into a deadly one with Smac mimetics."