But if people have a built-in tumor supressor, why do so many get cancer? The p53 molecule can be inactivated in several ways. In some human families, for example, p53 mutations are inherited, and family members have a high incidence of cancer. More often, the molecule is inactivated by an outside source. DNA tumor viruses, such as the human adenovirus and the human papilloma virus, can bind to and inactivate the p53 protein function, altering cells and initiating tumor growth. In addition, some sarcomas amplify another gene, called mdm-2, which produces a protein that binds to p53 and inactivates it, much the way the DNA tumor viruses do.
The p53 tumor suppressor and its surrounding molecules are now the focus of thousands of studies in laboratories around the world. These studies may one day lead to new treatments for the most frequent and life-threatening of cancers.
The tumor-suppressing p53 protein (left) can bind to target sequences on the DNA double helix to activate genes that prevent cell growth. Illustration courtesy of Stephen K. Burley.