Epigenetic modifications of chromatin and telomeres have an important effect in regulating how and when our genes are expressed. Previous studies have shown that telomere shortening occurs in pathological situations such as cancer and the aging process. However, until now little was known about the overall impact of these defects and what their mechanisms of action.

The National Cancer Centre (CNIO), Maria Blasco and her group of telomeres and telomerase have spent several years doing research on this particular class. Their results were published in journals of high impact and is not an exception one of his later works. In an article that appeared recently in Nature Genetics, Blasco and colleagues have used transgenic mice

with a deficiency in telomerase that cause a very short telomeres by coating the ends of their chromosomes. These mice suffer from a number of changes in the structure of the end of chromosomes, including defects in DNA methylation and histone acetylation causing the decompression of the genetic material of this region.

The loss of telomere compaction could lead them to be more accessible to telomerase and would enhance the activities of uncontrolled recombination and the appearance of deleterious mutations that favor uncontrolled tumor growth. Furthermore, this lack of compaction in telomeres and associated major changes in chromatin structure lead to alterations in the expression of genes that could play an important role in the evolution of carcinogenic processes

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