Nobel medicine prize laureates made public
Elizabeth Blackburn, Carol Greider and Jack Szostak jointly share the award.
Their work revealed how the chromosomes can be copied and has helped further our understanding on human ageing, cancer and stem cells.
The answer lies at the ends of the chromosomes - the telomeres - and in an enzyme that forms them - telomerase.
The 46 chromosomes contain contain our genome written in the code of life - DNA.
When a cell is about to divide, the DNA molecules, housed on two strands, are copied.
But scientists had been baffled by an anomaly.
For one of the two DNA strands, a problem exists in that the very end of the strand cannot be copied.
Therefore, the chromosomes should be shortened every time a cell divides - but in fact that is not usually the case.
If the telomeres did repeatedly shorten, cells would rapidly age.
Conversely, if the telomere length is maintained, the cell would have eternal life, which could also be problematic. This happens in the case in cancer cells.
This year’s prize winners solved the conundrum when they discovered how the telomere functions and found the enzyme that copies it.
Elizabeth Blackburn, of the University of California, San Francisco, and Jack Szostak, of Harvard Medical School, discovered that a unique DNA sequence in the telomeres protects the chromosomes from degradation.
Joined by Carol Greider, then a graduate student, Blackburn started to investigate if the formation of telomere DNA could be due to an unknown enzyme, and the pair went on to discover telomerase - the enzyme that enables DNA polymerases to copy the entire length of the chromosome without missing the very end portion.
Their research has led others to hunt for new ways to cure cancer.
It is hoped that cancer might be treated by eradicating telomerase. Several studies are underway in this area, including clinical trials evaluating vaccines directed against cells with elevated telomerase activity.
Some inherited diseases are now known to be caused by telomerase defects, including certain forms of anaemia in which there is insufficient cell divisions in the stem cells of the bone marrow.
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