The human body consists of fifty trillion cells, and each cell has 46 chromosomes which are the structures in the nucleus containing our hereditary material, the DNA. The ends of all chromosomes are protected by so-called telomeres.
The telomeres serve to protect the chromosomes in much the same way as the plastic sheath on the end of a shoelace. But each time a cell divides, the telomeres become a little bit shorter and eventually end up being too short to protect the chromosomes.
Each cell has a ‘multi-ride ticket,’ and each time the cell divides, telomeres will use up one ride. Once there are no more rides left, the cell will not divide any more, and will ‘retire.’ But some special cells in the body can activate telomerase, which again can elongate the telomeres.
Sex cells, or other stem cells, which must be able to divide more than normal cells, have this feature. Unfortunately, cancer cells have discovered the trick, and it is known that they also produce telomerase and thus keep themselves artificially young. The telomerase gene therefore plays an important role in cancer biology, and it is precisely by identifying cancer genes that the researchers imagine that you can improve the identification rate and the treatment.
“We have discovered that differences in the telomeric gene are associated both with the risk of various cancers and with the length of the telomeres. The surprising finding was that the variants that caused the diseases were not the same as the ones which changed the length of the telomeres. This suggests that telomerase plays a far more complex role than previously assumed,” said Dr Stig Bojesen from the University of Copenhagen, Denmark, first author of a paper published in Nature Genetics.
