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Institute of Bioengineering



Dr Cleo Bishop. Senescence - from young to old and back again.

Image: Cleo Bishop
Cleo Bishop

Date: 19 March 2014   Time: 15:00 - 16:00

Dr Cleo Bishop

With extended culture, normal human mammary epithelial cells (HMECs) eventually reach a state of stable proliferative exhaustion and enter a state of deep senescence, mediated by the cell cycle inhibitor p16INK4a. The acquisition of oncogenic mutation, either in early stage tumourigenesis, or in vitro, enables extended proliferative potential or immortality. Consequently, there is deep interest in determining the role of senescence in vivo in cancer. In addition, advancing age is the major risk factor for chronic diseases, a host of which have been associated with senescence, and in particular with p16INK4a. Given these connections between senescence, cancer and ageing we sought to explore the changes in the epigenomic landscape during senescence and to challenge to long-held dogma that senescence is an irreversible state of cell cycle arrest.

Key references

Cellular senescence mediated by p16INK4A-coupled miRNA pathways.
Overhoff MG, Garbe JC, Koh J, Stampfer MR, Beach DH, Bishop CL*.
Nucleic Acids Res. 2013 Nov 11.
Primary cilium-dependent and -independent Hedgehog signaling inhibits p16(INK4A).
Bishop CL*, Bergin AM, Fessart D, Borgdorff V, Hatzimasoura E, Garbe JC, Stampfer MR, Koh J, Beach DH.
Mol Cell. 2010 Nov 24;40(4):533-47.

Location:  PP1 Lecture Theatre