Cancer Hallmark #4. Unlimited Replication Potential

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The page below is a sample from the LabCE course Hallmarks and Signaling of Cancer Cells. Access the complete course and earn ASCLS P.A.C.E.-approved continuing education credits by subscribing online.

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Cancer Hallmark #4. Unlimited Replication Potential

Normal cells replicate, divide, and multiply but they also have an aging process. In other words, normal cells do not have unlimited growth potential. It has been documented that a typical cell undergoes approximately 50 rounds of cell divisions before they time out.
However, time out does not mean cell death. It simply means the cell division process slows down after about 50 rounds of divisions, and the cell becomes inactive. This inactivity is termed senescence. A senescent cell is inactive but very much alive.
How does senescence occur in normal cells? The clue comes from telomeres. Telomeres protect the ends of chromosomes from damage. In the absence of telomeres, each time a cell undergoes one round of division, the chromosomal ends are left exposed without protection.
However, telomeres do not last forever. In fact, after each cell division, the telomere shortens out a little, similar to a candle that has been burned. When telomeres are completely gone, chromosomal DNA damage is inevitable. When DNA damage is beyond control, p53 signals the cell to undergo apoptosis. Apoptosis is the intentional or programmed death of the cell.
Unlike normal cells, cancer cells are able to preserve their telomeres by activating a protective protein called telomerase.
Telomerase was discovered in 1984 by Dr. Carol Greider (now a professor at Johns Hopkins School of Medicine) and Dr. Elizabeth Blackburn (now President of the Salk Institute of Biological Sciences). Both scientists were awarded the Nobel Prize in Physiology or Medicine in 2009.