Baby cells are born when their parents divide in two. After they finish growing, cells make two copies of their genetic material, which they divide between their daughters when they themselves spit.

The cell operates a number of checkpoints to make sure it is in good shape before it copies its DNA. Once it does so it has set in motion the process of dividing in two and cannot turn back.

It is these checkpoints that usually ensure that cells with damaged DNA don't divide. But cancerous cells try to skip over the safeguards and divide faster and more often than they should.

Dr. Phillip W. Hines, assistant professor of pathology, draws an analogy between cells and cars to explain how the cell tries to fight cancer. The disease tries to put the normal cell machinery on overdrive. The cell can respond by destroying itself or by putting on the breaks--stopping its movement through the cell cycle. Cancers try to disable p53 because it plays a key role in both of these cancer-fighting mechanisms.

"The ability to act as breaks and the ability to act as an executioner are probably functionally distinct jobs of p53, but both of them have the same result: stopping an aberrant cell from dividing," Hines says.

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P53 stops cancer. And p73 looks a lot like it. When p73 was discovered, scientists were intrigued. Might it be involved in stopping cancer too?

Studies over the last three years have suggested that p73 is very different from its cousin. p53 is strongly expressed all over the body, but p73's expression is weak and variable. And p53 exists in only one form, but p73 seems to exist in several different forms.