A team of researchers at the Universitat Autònoma de Barcelona (UAB) has discovered a new mechanism that accelerates the shortening of telomeres (structures that protect the ends of chromosomes) involved in genetic instability and a predisposition to cancer. The research has been published in the journal Human Molecular Genetics.
DNA in higher organisms is organised into individual chromosomes, the ends of which are protected by structures called telomeres. Telomeres are very important in maintaining the cells’ genetic integrity, as they prevent the chromosomes from joining together, protect their ends from degradation and are involved in segregating chromosomes properly during cellular division. They also play a decisive role in two fields that are very important in social and biological terms: cancer and ageing. Telomeres gradually shorten and thus indicate the point at which the cell dies and control the proper proliferation of tissues.
For the first time, a team of researchers at the Universitat Autònoma de Barcelona has observed that telomeres may shorten more quickly due to sudden breakages in the DNA sequence that they consist of. The scientists made this discovery by analysing cells from a genetic syndrome called Fanconi’s anaemia, which is typified by a high genetic instability and chromosomal fragility, and which causes a very high predisposition to contracting cancer in harbourers (a risk of leukaemia 15,000 times higher than in a healthy person). The researchers have observed that the telomeres of affected patients present an accelerated shortening owing to breakages in the telomeric DNA sequence, leading to chromosomes being unprotected and joining together. This mechanism may explain patients’ symtomatology and their tendency to contract cancer. The research thus provides a first experimental link between a predisposition to cancer with the mechanism of sudden shortening of telomeres.
Octavi López Coronado | alphagalileo
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