Dear All,

It is my immense pleasure to invite you to the next Nencki Institute seminar, which will take place on the 9^th of March, at 3pm in the CN hall as usual.

This talk will inaugurate a new series - the “Ster lectures”. This new initiative aims to provide the PhD students with the opportunity to shape and impact the Nencki Institute Seminars by inviting their guests.

Next week, we will host prof. Richard GA Faragher who is a Co-Director of the BBSRC-MRC BLAST Network at the School of Applied Sciences of the University of Brighton. Prof.  Faragher will come by invitation of Grégory Petrazzo, a PhD student from the Laboratory of the Molecular Bases of Aging, led by prof. Ewa Sikora.

Prof Faragher will give a lecture entitled: Therapeutic opportunities presented by modulation of cellular senescence.

ABSTRACT

Cellular senescence is a permanent state of growth arrest coupled with profound changes in phenotype that can be triggered by multiple extrinsic or intrinsic stimuli. Senescence is a process-level example of the evolution of ageing mechanisms through antagonistic pleiotropy and plays a primary role in tumour suppression, although evidence is mounting for its involvement in other fundamental physiological processes.

Evidence from our laboratory on human premature ageing diseases complements data from transgenic mice in which it is possible to specifically delete senescent cells and are consistent with a model in which the accumulation of senescent cells through the life course is responsible for later life chronic disease and impairment. The removal of senescent cells or their reversion to a phenotypically benign state is thus an important emerging goal of translational medicine.

Modern bioinformatic approaches based on text mining have allowed an impartial ranking of the impairments most closely associated with this process. Whilst many groups are now working on the ablation of senescent cells our laboratory has demonstrated that it is possible to revert them their primary phenotype with polyphenolics or inhibitors of p38 MAP kinase. Lastly, the potential for senescence to act as a barrier to the development of bioartificial organs designed to treat some of these conditions is discussed as are the approaches we have developed to overcome it.

The seminar will be followed by a get together.

With best regards,
Aleksandra Pękowska