We are used to thinking that our cells will try every attempt to repair DNA damage, and escape the apoptosis fate that awaits them if they do not do so. We are also used to thinking that evolution works against those cells that dont attemp to escape their fate.

That is not always the case, though. This classic view may not be valid for all kinds of DNA breaks, as shown in the talk by Fabrizio d'Adda di Fagagna (receiver of the prestigious EACR young researcher award in 2009) during the session devoted to "Senescence & Ageing" in the second day of EACR conference in Oslo.

It seems that our concepts related to telomeres need to be updated, as in only two days both the talks by Elizabeth Blackburn (see: "Furry mice and bricklayers: more jobs for telomerases") and Fabrizio d'Adda di Fagagna stressed the need to revise our views on senescence and ageing due only to telomere shortening.

There were two important take-home messages in d'Adda di Fagagna's talk: not all kinds of DNA damage are the same, and our cells do not attempt to repair all types of DNA damage. This has implications for our understanding of the mechanisms that trigger senescence and ageing in mammalian cells.

The group led by d'adda di Fagagna at IFOM, Milan proved the hypothesis on the existence of "irreparable" DNA both in vitro and in vivo. In vivo, experiments showed that irreparable DNA damage persists in a cell model of terminally differentiated cells, namely hippocampal neurons exposed to X-ray DNA damage.

What is, then, the significance from an evolutionary point of view of cells which do not repair DNA damage? D'Adda di Fagagna put it thus: we always have to keep in mind that different evolutionary and selective pressures may act on different cells, and on different subcellular components of the same cell, thus allowing for the shaping of conditions that confer DNA repair resistance.

These findings have also implications for ageing, as evidence of DNA damage response (DDR) accumulation in primates needs to be rethought. There is no hard evidence that senescence and ageing are necessarily due to telomeres shortening. Indeed, it could be triggered to accululation of unrepaired DNA damage. Some preliminary data on primates point in this direction.