Molecular mechanisms of ageing Lecture Series We’re getting older…

Molecular mechanisms of ageing

  1. The event took place on
María Blasco

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  1. María BlascoMaría BlascoNacida en Alicante, obtuvo su doctorado en el Centro de Biología Molecular "Severo Ochoa" bajo la supervisión de Margarita Salas. Desarrolló su trabajo posdoctoral en el laboratorio de Cold Spring Harbor (Nueva York), liderado por la premio Nobel de Medicina, Carol W. Greider y desde entonces su investigación se ha centrado en la telomerasa y los telómeros.  En 1997 retornó a  España e inició  su propio grupo de investigación en el Centro Nacional de Biotecnología en Madrid. Posteriormente se trasladó al Centro Nacional de Investigaciones Oncológicas (CNIO)  que actualmente dirige. María Blasco ha recibido prestigiosos premios y galardones, entre los que destacamos: en 2004, la medalla de oro concedida por EMBO (European Molecular Biology Organization), en 2007 el Premio Rey Jaime I a la Investigación Básica y en 2010 el Premio Nacional de Investigación Santiago Ramón y Cajal.

Cancer and aging are travel companions. In a first view this relation may seem awkward, but the events that have allowed to establish this improbable bond go back to the year 1951 when for the first time it was possible to keep in lab culture conditions an immortal human cellular line, of cells that are in constant growth. The same barriers that separate normal cells from immortal cells connect in an intimate way the "how" with the "why" of aging.

The complexity of aging and biological cancer prevent from being able to extract easy generalizations. Cancer and aging are fostered by the accumulation of cellular damage. Those mechanism protecting the cells from damage will provide protection for both cancer and aging. On the other hand, cancer and longevity require a durable potential of cell proliferation and, thus, the mechanisms limiting the indefinite cell proliferation (like for example the telomeric shortening or cellular senescence) will provide protection against cancer, but a the same time favor aging. The net equilibrium between these two types of mechanism, those diminishing the amount of cell damage (protecting at the same time from cancer and aging) and those preventing from the excessive cell proliferation (which normally do not limit the average life of the individual, but that in protected environments may contribute to aging) would be what would ensure a healthy existence (free of cancer and of the complications derived from aging) to most individuals during the young and adult life periods.