Jerry W. Shay, a professor of cell biology at the University of Texas Southwest Medical Center and a leading telomerase researcher, offers this explanation:

TELOMERES, seen here in red, cap the ends of chromosomes and erode with each successive division in normal cells. Cancer cells, however, maintain their telomeres with the help of the enzyme telomerase.
In 1972 geneticist James Watson discovered that, because of the way DNA replicates, our chromosomes have a problemone he called the "end replication problem." Each time a normal human cell divides, its telomeresenzyme caps that protect the ends of the chromosomes like plastic shoelace tipsget progressively shorter. Eventually the telomeres dwindle to the point where the cell can no longer replicate.

A hallmark of most cancer cells is that they divide indefinitely. In order to do so, they must figure out a way around these short telomeres. As it turns out, the cells accomplish this feat by reactivating an enzyme called telomerase, which adds new telomeres onto the ends of chromosomes to compensate for the end replication problem. Telomerase is expressed during early human development but remains silent in almost all adult tissues. Human cancers, in contrast, express telomerase, which maintains their telomeres at a stable and usually very short level. Because of this fact, the cells can replicate indefinitely.

Inhibition of telomerase may thus represent a novel anticancer therapeutic approach. If we can suppress telomerase, we may be able to drive cancer cells into a growth arrest state. Many laboratories, including my own, are studying this at the present time, and the preliminary results are very encouraging.