HealthScout

In a bit of sour news for immortality buffs, researchers have found that trying to prolong cell life by keeping chromosomes from eroding may lead to cancer.

While the finding doesn't prove that these anti-aging efforts cause cancer, it does run up a caution flag for scientists trying to slow aging at the cellular level.

"You don't have perfect control over the conditions" of cell growth, says Gregory Hannon, a researcher at Cold Spring Harbor Laboratory and a co-author of the report. It appears in the British science journal Nature.

The work involves tinkering with the fringes of chromosomes, the DNA structures that make up genes. The ends of chromosomes are long strings of DNA that act in essence like molecular shoelace tips, protecting the valuable genetic information deeper in the bundle. Each time a cell divides, it sheds a bit of this protective telomere, until the more essential sections of the chromosome are in jeopardy and the cell dies.

In recent years, scientists have shown that blocking the erosion of telomeres with an enzyme called telomerase gives cells a reprieve. Telomerase, by adding DNA to chromosome ends with each division, enables cells to divide, if not indefinitely, then for far longer than they otherwise would.

Earlier studies have also found that this technique doesn't appear to make cells divide too much, becoming cancerous. But the latest work hints that tinkering with telomeres might not be so benign, after all.

Hannon's group infected mature, but dying, human breast tissue with a virus that had been altered to produce telomerase. As expected, the treatment "immortalized" the cells, keeping them dividing well past their usual demise at 50 to 60 doublings.

When they deleted the viral gene, however, the doubling didn't stop immediately, suggesting that the cells' normal telomerase system had been reactivated. And indeed, Hannon and his colleagues found signs that a cancer gene called c-myc had become over-expressed by two to three times its normal level. C-myc is known to trigger telomerase.

Although the researchers didn't see direct evidence of cancer in the altered cells, they did find that the levels of c-myc in the treated tissue was similar to that in breast tumor samples.

Dr. William Hahn, a cancer researcher at the Whitehead Institute for Biomedical Research at the Massachusetts Institute of Technology, says although the latest work has a few technical gaps, "I agree with the take-home message: Tissue engineering with cells immortalized with telomerase is something we need to be very, very careful with."

The immense appeal of the technology -- with applications ranging from skin grafts to a universal cancer vaccine -- reinforces the need to tread carefully, says Hahn.

Abnormal c-myc activity is found in some 70,000 deadly human cancers a year. The gene is normally involved in cellular housekeeping, Hannon says, but gets co-opted by cancer to spur unchecked division.

What To Do

This research is in the very earliest stages, so don't look for the fountain of youth for years -- if ever.
　　(From Bell South)