When good genes go bad

DNA mysteries: Advances in medicine must take into account the paradoxical roles of many genes.

January 10, 2002

MAPPING the human genome, or genetic blueprint, has kindled hope that we can eventually select the genes we like and replace or suppress the ones we don't.

But nature often has a good reason for keeping those bad genes and their proteins, and maintains a delicate balance of benefit and harm. Natural selection, it turns out, doesn't mean eliminating all the apparently unwelcome elements, because they may also have hidden virtues.

That's what scientists at Baylor University found when looking at a protein known to be a potent cancer-fighter. This protein also triggers the effects of aging. So drug therapy aimed at turning on the fountain of youth may weaken the body's defenses against cancer. And chemotherapy against cancer in young people may accelerate the body's aging process.

Scientists are aware of the ambivalent character of some other disease-related genes.

The gene that causes sickle-cell anemia, for example, also affords resistance to malaria. Similarly, the gene that causes Tay-Sachs disease is thought to defend against tuberculosis.

Perhaps 1,000 of these kinds of gene-linked disorders, most of them rare, have been identified. Their early prediction by genetic typing can lead to improved treatment. Trying to eliminate the harmful gene could have serious unforeseen effects.

As the Baylor study of the cancer-fighter, aging-promoter protein p53 suggests, there may be many doubled-edged swords in the body's complex arsenal.

Better understanding of disease and the body's mechanisms can lead to the development of better therapies. Because the genetic building blocks can have multiple purposes, these efforts will require much more than a simple blueprint.

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