Telomerase is the key to cancer cells’ longevity – and an unambiguous target
| Every time a cell divides itself to create two new cells (a process called mitosis), it must first replicate its DNA into two identical copies. The way this replication is conducted means that with each cell generation, the edges of our chromosomes become slightly shorter. This is why their end parts are composed of telomeres, regions of repetitive, non-coding DNA, which our chromosomes can afford to lose without suffering any damage.
For normal cells, a large number of divisions will eventually deplete the telomeres, meaning more replication cycles would damage coding DNA and result in malfunctioning proteins. This is known as the “Hayflick limit”, and is believed to occur after 50 to 70 division cycles. As it can no longer function properly, the now-« old » cell will die through a process call apoptosis (programmed cell death). |
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Cancer cells, on the other hand, will produce an enzyme called telomerase, or more formally human telomerase reverse transcriptase (hTERT), which adds non-coding DNA to the telomeres at the end of each replication cycle. Consequently, the telomeres never get shorter, and coding DNA is protected. This is why cancer cells are called « immortal »: they do not get older and can replicate an infinite number of times, in the proper conditions. As an example, the line of human cancerous cells called HeLa cells has been used in research since 1951. However, hTERT inhibition induces their death.
Because hTERT is almost exclusively found in tumor cells, and is critical to their survival, the immune system can be trained to recognize and kill cancerous cells without harming healthy ones. The purpose of our IVS-2001 vaccine is to trigger an immune response against telomerase. |
Telomerase is overexpressed in >90% of human cancers, making it a near-ubiquitous target for immunotherapy.
A glossary is available for technical definitions.
