Escape from oncogene-induced senescence

The manuscript provides evidence on how senescent cells escape from oncogene induced senescence, an important tumor suppressor mechanism, facilitating tumor progression. Particularly the authors demonstrate that a recurrent chromosomal inversion harboring the circadian gene BHLHE40 is sufficient to drive escape from oncogene-induced senescence. The inversion is the outcome of oncogene-mediated genomic instability followed by chromatin refolding changes that activate the gene, leading to cell cycle re-entry and aggressive behavior. These findings support that replication stress-induced genomic instability is the causative factor underlying ‘‘escape’’ from oncogene-induced senescence and that targeting senescent cells can be of major clinical importance by eliminating a potential source of recurrence.

VG New

Prof. Vassilis G. Gorgoulis

Laboratory of Histology-Embryology
Molecular Carcinogenesis Group
Medical School
National and Kapodistrian University of Athens

 

 

Chair of Clinical Molecular Pathology,

Ninewells Hospital and School of Medicine

 

University of Dundee, Dundee, UK

 

Biomedical Research Foundation of the Academy of Athens

 

Faculty Institute for Cancer Sciences, University of Manchester,
Manchester Academic Health Science Centre, Manchester, UK

Manchester Centre for Cellular Metabolism,
University of Manchester, Manchester Academic Health Science Centre, Manchester

 

EMBO member

 

European Academy
of Cancer Sciences member

 

Academia Europaea member

 

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