Earlier this year Medical School Professor Frank McKeon genetically engineered mice that lack p73 to see whether they would develop cancer, just as mice that lack p53 do. The mice had "profound" defects in their metabolism and their nervous systems, but no tumors.

But other data suggests that the protein might be involved in cell death. Part of how p53 works is by attaching to different parts of the cell's DNA; in test tubes, p73 attaches to those same regions. It is located in a region of human chromosome 1 that is often damaged in cancer.

The Protein Was a Killer

Advertisement

In the most promising finding, Kaelin's group showed that p73 could be coaxed into substituting for p53 to induce death in cells lacking p53. This result surprised even Kaelin, who expected that p73 did not play a role in cell death based on all of the previous work.

The hunt was on to find the signals that normally operate to activate p73.

Kaelin's new experiments offer an intriguing preliminary answer; they show that a particular common protein spurs both p73 and p53 to do their jobs.

Taken together, Kaelin's results suggest that there are both usual and backup cell death pathways. p53 is a "professional tumor suppressor" and p73 is its understudy.

"Under normal conditions p73 is not a professional tumor suppressor," he said. "But if we are smart enough we might be able to make it act like one."