Scientists have cured cancer cells of their disease, turning them back into normal cells. They did it by injecting into the cells a normal regulatory gene that they lacked.

While the method cures individual cells, it would be impossible to inject all the millions or billions of cancer cells in a human victim. A single missed cell could proliferate and reestablish the disease. The method does, however, suggest a possible treatment.

The gene is one that tells cells how to make a protein called p53 (the number stands for the protein's molecular weight of 53,000 daltons). The protein plays a critical growth-regulating role within the cell. Absence or mutation of the p53 gene has been detected more often than any other genetic abnormality in cells of malignant tumors, including colon cancer, breast cancer, and tumors of the brain, lung and bone.

Normal cells contain two copies of the gene. In about 75 percent of colon cancers, one copy contains a mutation that spoils its protein product and the other is missing entirely.

Scientists at Johns Hopkins University School of Medicine and Case Western Reserve University wondered what would happen if they used genetic-engineering techniques to put back a normal copy of the p53 gene into colon cancer cells growing in a laboratory.

As soon as the cells received the gene, they stopped multiplying in the uncontrolled fashion typical of cancer cells. They resumed the behavior of normal cells, which stop multiplying when they reach a certain level of crowding.

In contrast, inserting a mutant copy of the gene had no effect on growth. Tiny amounts of the regulatory protein made by the gene were apparently able to bring the cancer cells' uncontrolled growth to a screeching halt.

While injecting cells is impractical as a treatment -- replacing the damaged p53 gene in every cell of a colon cancer tumor is technically impossible, said Suzanne J. Baker, a Hopkins graduate student and lead author of the report in last week's Science -- scientists may be able to develop a drug that mimics the regulatory protein's effect.

The five-member research team was led by Hopkins's Bert Vogelstein.