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Scientists restore gene to shrink tumors in mice
2007-01-24
Reactivating a gene that normally suppresses the growth of tumors may be an effective way to treat cancers, scientists said on Wednesday. The gene called p53 is a leading tumor suppressor which stops damaged cells from dividing. In the majority of human cancers the gene does not work properly. But teams of scientists in the United States have shown that reactivating, or restoring the function of the gene, can make certain types of tumors in mice shrink or disappear. "If we can find drugs that restore p53 function in human tumors in which this pathway is blocked, they may be effective cancer treatments," said David Kirsch of the Massachusetts Institute of Technology (MIT), a co-author of one of the studies published in the journal Nature. A fault in the p53 gene is one of many mutations that enable cancers to develop. But the gene is a major player in the disease because it controls a pathway, or chain of events, that helps cells deal with DNA damage. "If mice and humans respond in the same way to restoration of p53 this could be an important breakthrough," Andrea Ventura, of MIT, said in an interview. GENETIC TOOLS The role of p53 in cancer has been known for many years but until quite recently scientists have not had the genetic tools needed to do the types of studies reported in the journal. When p53 is working it controls the cell cycle and makes sure that mutated cells destroy themselves and do not divide uncontrollably to cause tumors. If the gene is mutated or inactivated the control mechanism doesn't work. The MIT scientists used genetically engineered mice who had cancerous tumors and an inactivated p53 gene which could be switched back on by a particular chemical. After they restored the function of the gene in the rodents most of the tumors decreased in size from 40 to 100 percent. "We have shown that if we restore the function of this gene in a tumor that is already grown and established we can induce tumor regression in the vast majority of cases," said Ventura. In a separate paper in the journal, Scott Lowe of the Cold Spring Harbour Laboratory in New York and his group used a technique called RNA interference in mice to achieve the same result. Reactivating p53 did not damage healthy cells in the rodents so any drugs developed to restore the activity of the gene may not produce toxic side effects. Both teams of scientists, who looked at different types of tumors in mice, found not all cancers responded in the same way to restoring p53. In mice with lymphoma, a cancer of the white blood cells, the cancerous cells died very quickly. But in mice with sarcoma, cancer of connective tissue, the cancerous cells went into a state of senescence, or stopped growing, when p53 was reactivated. Lowe's team, who looked at liver cancer, also saw senescence but the arrested cells were quickly cleared by an immune system response.
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