SUICIDE is a part of life. Whenever any of the 100 trillion or so cells that make up the human body malfunction, which happens all the time even in healthy tissue, they are programmed to provoke their own death. The mechanism hinges on a protein called TRAIL, which is produced by the damaged cell and binds to receptors on its surface, causing inflammation. That is a signal for the immune system to sweep in and, through a process called apoptosis, break down the damaged cell and recycle its parts to feed healthy ones. If this self-destruct is subverted, however, the result is a tumour.

When TRAIL's tumour-suppressing ability was first discovered in 1995 researchers hoped that by discriminating between cancer cells and healthy ones, TRAIL would do away with the debilitating side-effects associated with traditional treatments like radio- and chemotherapy. These are good at destroying tumours but also cause lots of collateral damage. Unfortunately, it turned out that simply injecting a synthetic version of the molecule into the patient's body provoked only a limited immune response in a handful of cancers.

That, says Joshua Allen from the Pennsylvania State Cancer Institute, was because people assumed that cancer's subversion of TRAIL consisted merely in halting the molecule's production within the cell. It turns out, however, that cancerous cells also suppress their TRAIL receptors, so no amount of synthetic TRAIL sloshing about would ever be enough. What you need, Dr Allen reasoned, is something to reboot the TRAIL-producing pathway within cells as well as to unblock their TRAIL receptors. Only then would the immune system be spurred into action.

So he and his colleagues sifted through a library of molecules maintained by America's National Cancer Institute and found a molecule, called TIC10, whose biochemistry seemed to fit the bill. When enough of these molecules accumulate in a cancer cell, they activate a protein called FOXO3a. This binds to DNA and flips on many biological pathways, including those involved in the TRAIL mechanism that lead to the immune-system alerting inflammation.

As Dr Allen and his colleagues report in Science Translational Medicine, tests in mice with brain tumours confirmed the biochemical hunch. Murine subject given TIC10 lived twice as long as those that received no treatment. The drug also worked for lymphoma, as well as breast, colon and lung cancers. And it did not seem to cause the wasting side-effects typically associated with chemotherapy, suggesting that it can indeed tell cancer cells from healthy ones. As an added bonus, TIC10 is small compared to TRAIL, and cheaper to concoct than the complex protein is.

Last year Dr Allen secured a $1.3m grant from Pennsylvania's department of health to begin clinical trials. These will be carried out in collaboration with Oncoceutics, a drug company. Nine out of ten promising molecules which work in mice fail in humans, so "Cure for cancer" headlines must wait. If TIC10 does live up to its promise, though, it would make one killer app.