By Sean Henahan, Access Excellence

WASHINGTON, D.C. (10/18/96) Dramatic therapeutic results against human cancers grown in laboratory mice suggest that mutated versions of a common cold virus might be used to treat various human tumors.

Researchers managed to enlist the adenovirus in the fight against cancer by exploiting an inherent characteristic of the virus. Adenoviruses encode a protein that binds to and inactivates a well known tumor suppressor protein called p53. The researchers found that deleting the gene for the protein prevented the virus from reproducing in normal cells, but not in cancer cells lacking the p53 tumor suppressor gene.

Studies in mice have now shown that injecting the modified virus inhibits the growth of transplanted p53-deficient human cancers. Indeed, the mutant virus killed p53-deficient tumor cells 100 times more efficiently than can normal cells containing functional p53. This is considered especially good news among cancer researchers, since native cells lacking p53 or containing ineffective p53 are believed to contribute to the develop of at least 50% of all human cancers.

"Injection of the mutant virus into p53-deficient cancer cells caused a significant reduction in tumor size and caused complete regression of 60 percent of the tumors. These data raise the possibility that mutant adenoviruses can be used to treat certain human tumors," the researchers reported in Science.

"What I like is how clever it is," commented Richard Klausner, director of the National Cancer Institute in Bethesda, Maryland. "It's been a long-held fantasy to find an [anti-cancer] virus."

The P53 gene's regular job is to detect flawed DNA (such as would be found in cancer cells or viral DNA) when cells divide. P53 either halts the cell division long enough for DNA repair to take place, or initiates a process of programmed cell death (apoptosis) in the faulty cell.

Preliminary clinical studies are now underway testing the adenovirus strategy. Patients with head and neck tumors receive injections of the virus directly into the tumor. The first results are expected in the Spring of 1997.