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Mortality Molecules


Credit: Svislo/istockphoto

By Tracy Bryan

Cancer cells become immortal by exploiting a mechanism that protects normal cells from DNA damage. Can we use these molecules to turn off cancer’s fountain of youth?

The full text of this article can be purchased from Informit.

Our genomes are subjected to a plethora of potentially damaging insults over the course of our lifetimes. Oxidative damage, irradiation, chemicals, and errors that occur when the genome is copied during cell division can lead to nicks, breaks and other damage to DNA.

Cells have evolved various “sensor” molecules to respond to this DNA damage, leading to either repair of the damage or cellular “suicide” if the damage cannot be repaired. This is an important safeguard that helps to prevent our normal cells from becoming cancerous.

In cancer cells, however, these responses to DNA damage are often defective, leading to the accumulation of mutations that can promote cancer cell division. We now know that cancer cells have yet another trick up their sleeve – they can also exploit these DNA damage-signalling molecules to keep the ends of their chromosomes long, essentially endowing themselves with immortal life.

The aspect of cell biology that has most fascinated me for the past 20 years is the process by which normal cells sense the fact that they are ageing. The ends of our chromosomes, known as “telomeres”, gradually shorten with each cell division over time. This process acts like an elegant biological “clock” that tells the cells of our body to age.

However, cancer cells counteract this clock and keep growing out of control. They use an enzyme...

The full text of this article can be purchased from Informit.