Most of the body's cells end life dramatically: upon completing their biological tasks or sustaining damage, they kill themselves. Failure to do so can lead to an accumulation of excess cells, each of which has the potential to mutate into a cancerous cell. Previous research had shown that a protein dubbed p53 instructs cells with faulty DNA to commit suicide. According to reports published today in the journal Nature, two more proteins have now emerged as important players in this process.

In the first study, led by William G. Kaelin of the Dana-Farber Cancer Institute, the researchers set out to determine whether a protein called E2F-1, which was known to activate p53, could also prompt its close relative, p73. Earlier work had indicated that a number of proteins that activate p53 do not affect p73, but by employing tumor cells that lacked p53, the team found that E2F-1 does, in fact, activate p73. Furthermore, it appears that the two tumor suppressors work together to induce cell death.

Building on Kaelin's findings, Washington University pathologist Steven F. Dowdy and his colleagues focused on suicide in immune system cells called T cells, a process known as T cell receptor activation-induced cell death (TCR-AICD). Their research revealed that T cells lacking either E2F-1 or p73 genes fail to undergo TCR-AICD. Such malfunctioning can lead to lymphomas, leukemias and autoimmune diseases. "When a particular receptor is stimulated, it activates E2F-1, which turns on the p73 protein." Dowdy explains. "Then p73 activates the machinery that causes that cell to die." The studies may inspire new cancer treatments. Indeed, Kaelin notes that it might one day be possible to eliminate many cancers by activating the p73 gene directly.