Scientists may have found way to 'immortalize' cells Research may open path to treating a variety of degenerative diseases

January 14, 1998|By LOS ANGELES TIMES

Breaking a biological barrier once thought out of reach, scientists have for the first time endowed healthy human cells growing in a dish with a quality that alchemists, explorers, and mystics have sought for ages: immortality.

The research, to be published Friday in the journal Science, opens a new path to the treatment of cancer and a variety of HTC degenerative ailments, including heart disease and age-related vision loss. Such "immortalized" healthy human cells might also serve as biological factories for churning out genetically engineered drugs.

Most tantalizing, scientists say, the finding offers a glimpse of the molecular gears and springs that make up the biological clock, thus renewing hope that the limit of the human life span may not be absolutely fixed after all.

The new study -- by scientists at Geron Corp. in Menlo Park, Calif., and the University of Texas Southwestern Medical Center in Dallas -- is "an important discovery," said Anna McCormick, chief of the biology of aging program at the National Institute on Aging. "It opens another door to understanding the mechanisms of aging at the cellular level."

Leonard Hayflick, a cell biologist at the University of California at San Francisco who pioneered the field nearly 40 years ago, said the study represented a "monumental advance in understanding the genetics of aging." Hayflick, a member of Geron's scientific advisory board, said he never thought he would see such progress. "I'm just amazed," he said.

The study addresses a question that has been at the center of aging research since Hayflick and his co-workers discovered that most healthy animal cells are programmed to divide a particular number of times before they reach the end of the line and stop dividing, a crucial step in aging.

The new research supports the idea that an animal cell's innate "division potential" is largely controlled by a particular stretch of DNA, called telomeres, at the tips of chromosomes. Each time a cell divides, a chunk of telomere is snipped off. Dividing ceases when the telomere is shortened to a particular amount.

As simple as the "telomere-clock model" sounds, proponents have found it impossible to prove -- until now. The Geron and Texas researchers used a gene that blocks telomere shortening and inserted it into laboratory cultures of two healthy human cells -- retina cells and a type of skin cell. The altered cells kept on dividing long after the unendowed versions of the same cells reached the end of the line.

The results are "strikingly unequivocal," Titia de Lange, a cell biologist at Rockefeller University in New York City, wrote in an accompanying editorial.

Pub Date: 1/14/98

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