Apoptosis, a process built into most healthy cells, causes them to die if something goes wrong -- the procaspase-3 protein turns into the enzyme caspase-3, which initiates cell death.

But cancer cells don't behave that way -- the procaspase-3 protein doesn't get the message that something is wrong, and therefore does not make the transformation. That allows the cancer cells to grow into tumors. The synthetic compound, however, prods the cancer cells to self-destruct.

In their study, chemistry professor Paul J. Hergenrother and colleagues at the U of I's Urbana-Champaign campus discovered that a compound called "procaspase activating compound one," or PAC-1, killed cancer cells in 23 tumors of a variety of cancer types.

The PAC-1 tricks procaspase-3 into generating caspase-3, causing cellular suicide, they observed. It did not cause healthy cells to self-destruct at a higher rate than normal, nor did it have any other negative effect, the investigators said. In fact, cancer cells are two thousand times more sensitive to PAC-1 than non-cancerous cells, they pointed out.

The study, which involved the examination of cell cultures and mouse models, is published in the journal Nature Chemical Biology.

"This is the first in what could be a host of organic compounds with the ability to directly activate executioner enzymes," said Hergenrother. "The potential effectiveness of compounds such as PAC-1 could be predicted in advance, and patients could be selected for treatment based on the amount of procaspase-3 found in their tumor cells."

Such personalized medicine strategies are preferred over treatments that rely on general cytotoxins, the researchers note, and could be the future of anti-cancer therapy.

Further research involving human test subjects will be required to determine the efficacy and possible side effects of employing a similar treatment approach with humans.