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IMMORTALITY, (excerpt)
 Dr. Ben Bova

The Hayflick limit

In the 1970s the American cellular biologist Leonard Hayflick discovered that most types of human cells have a natural limit to the number of times they can divide, or reproduce. 

Some types of cells, such as those that produce red and white blood corpuscles, can divide millions of times. Others, such as most nerve cells, do not reproduce at all. If a cell's Hayflick limit is 50, for example, it will divide 50 times and then become senescent. It withers and dies.  When enough of our cells die, we die. 

["senescent" means "old."]

Immortal cells

Some cells have no Hayflick limit. Barring trauma from outside, they are immortal. They can be killed, but they do not age.  The "lowly" bacteria are immortal. They can be killed -- by starvation, radiation, lack of water, or being eaten by another organism. But they do not age. Bacteria keep on dividing forever, until some outside agency kills them. 

Cancer cells are similarly immortal. They keep on dividing and dividing, endlessly, unless they are killed or their host dies. "HeLa" cells, taken from the tumor of Henrietta Lacks in 1951, are still reproducing as vigorously as they did nearly 50 years ago. 

Human germline cells -- ova and sperm cells -- also show no Hayflick limit. 

Why can some cells keep on going and going like the pink bunny in the TV commercials, while others curl up and die after a certain number of divisions? 

Telomeres

Some biogerentologists (scientists who study aging) believe the answer lies in our telomeres. 

Inside the nucleus of virtually every cell in your body are the long strands or filaments called chromosomes. Human cells have forty-six chromosomes, except for the sex cells, which have half that number. The chromosomes contain DNA. DNA makes up the cell's genes. 

At the tip of each spindle-shaped chromosome is a sort of cap, called a telomere. Telomeres somewhat resemble the aglets on the ends of shoelaces. The telomeres keep the ends of the chromosomes from sticking together, and from sticking onto other chromosomes. Bacterial DNA does not have telomere caps, and tends to loop itself into a ragged circle, like a snake swallowing its tail. Telomeres keep the individual strands of DNA in our cells from looping or connecting to one another. They also play an intriguing role in cellular aging. Some researchers believe that telomeres are a sort of cellular clock that sets the rate at which the cells age and eventually die. Each time a cell divides, its telomeres shorten. When the telomeres become short enough, cell division stops and the cell soon dies. But cancer cells regrow their telomeres after every division.  Michael Fossel, professor of clinical medicine at Michigan State University, says quite clearly, "Telomeres [are] the clocks of aging." He and other researchers believe that telomere shortening is responsible for cellular aging and, eventually, cellular death.  Most biologists do not accept so simple an explanation. And yet... 

Telomerase

In January 1998 researchers announced that they had extended the lifespan of human cells "indefinitely" in a laboratory experiment in which telomerase was added to the cells. Telomerase is the enzyme that essentially builds new telomeres. 

Cancer cells produce plentiful telomerase. Normal human cells do not -- even though they have the telomerase gene in their DNA. In normal human cells, that gene is suppressed, deactivated.  The researchers, from Geron Corporation and the University of Texas Southwest Medical Center, inserted an activated telomerase gene into the cells. The cells reproduced well past their Hayflick limits, giving powerful evidence that telomeres have a decisive influence on cellular senescence and may indeed be "the clock of aging." 

Writing in the prestigious journal Science, biologist Titia de Lange, of Rockefeller University's Laboratory for Cell Biology and Genetics, commented, "The doubt [about telomeric influence on aging] has now come to an end with a report...describing direct evidence for a causal relation between telomere shortening and cellular senescence." 

Telomerase and Cancer

Many researchers are interested in finding how to prevent cancer cells from producing telomerase. If a telomerase "off" switch could be found, it will become possible to stop tumors before they grow large enough to be trouble. 

The fact that normal cells possess the telomerase gene but do not employ it may be a warning signal. Activate that gene and the cell may start runaway cancerous growth. 

The goal, then, is to control telomerase production well enough to remove the cell's Hayflick limit and allow the cell's owner -- maybe you! -- to live forever. Without causing cancer. 

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