Narrator: This is Science Today. One of the mysterious mechanisms of a promising, experimental anti-cancer drug has been solved. The drug - which is a genetically modified cold virus - works by targeting cells that have a defective tumor suppressor gene called p53. But in clinical trials, it was discovered the experimental drug was also working against cells in which p53 was intact. The drug's creator, Frank McCormick, of the University of California, San Francisco, says this didn't jibe with the original theory.
McCormick: The original idea was that this virus could only grow in tumor cells that lack functional p53 - that's what allows it to grow.
Narrator: The researchers speculated something else was wrong with the p53 in those cells. And that something else turned out to be a loss of a protein called p14, which regulates the p53 gene. So, McCormick says their experimental drug works on more cells than previously thought.
McCormick: We thought originally, sixty percent of human tumor cells have mutation in p53, but now we know that probably eighty to ninety percent of tumors have some defect in the p53 pathway.
Narrator: For Science Today, I'm Larissa Branin.