Cellular senescence is a state in which cells limit their proliferation in response to stress, DNA damage or in a programmed manner. It was initially described more than half a century ago, but in recent years research has shown the key role of this process in various physiological contexts, from pathologies such as cancer or fibrosis, to embryonic development. The activation of senescence causes, in the first instance, that the cell stops dividing and, eventually, can lead to its elimination mediated by the immune system. Today we know that cellular balance, in a great variety of physiological and pathological situations, depends to a great extent on the correct functioning of cellular senescence. For this reason, errors in this balance, by excess or by defect, can have dramatic consequences, such as malformations during development or the formation of tumors.

Cancer is a disease characterized by the uncontrolled proliferation of cells of a specific tissue, which have the capacity to invade and destroy these and other tissues by the formation of neoplasms (2). This pathology originates from the deregulation of cellular homeostatic mechanisms, which lead to cells that can alter the cell cycle and evade the pathways of apoptosis.

Although cellular senescence and cancer appear to be opposite processes, they have common molecular mechanisms such as the accumulation of DNA damage, genomic instability, the presence of mutations and / or deregulation of genes involved in the cell cycle. Our research group is interested in evaluating the presence of epigenetic mechanisms that control these processes.

For the execution of this proposal we work in a network with the researcher Berta Cristina Henríquez, PhD and professor of the Faculty of Science of the San Sebastian University (Chile).




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