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One of the most important molecules relating to cancer is called p53. This Click and Learn explains the structure and function of the p53 protein as well as how the protein's activity is regulated. Learn why p53 is called the guardian of the genome and how interfering with its function can lead to cancer.

She wanted to understand the effects of mutations that the gene for p53 is prone to. In dozens of simulations, she and her colleagues tracked how common p53 mutations further destabilize the already floppy protein, distorting it and preventing it from binding to DNA. Some simulations also revealed something else: a fingerhold for a potential drug. Once in a while, a small cleft forms in the mutated protein's core. When Amaro added virtual drug molecules into her models, the compounds lodged in that cleft, stabilizing p53 just enough to allow it to resume its normal functions.

In 1977, a University of Oxford statistician named Richard Peto pointed out a simple yet puzzling biological fact: We humans should have a lot more cancer than mice, but we don't. Dr. Peto's argument was beguilingly simple. Every time a cell divides, there's a small chance it will gain a mutation that speeds its growth. Cells that accumulate several of these mutations may become cancerous. The bigger an animal is, the more cells it has, and the longer an animal lives, the more times its cells divide. We humans undergo about 10,000 times as many cell divisions as mice - and thus should be far more likely to get cancer.

Elephants have evolved extra copies of a gene that fights tumour cells, according to two independent studies, offering an explanation for why the animals so rarely develop cancer.