International Cell Senescence Association
The association aims to promote research, co-operation and exchange of information among all those interested in any aspect of cellular senescence.
Cellular senescence is a programmed state of stable cell cycle arrest that is accompanied by a complex phenotype. Senescent cells play a role in physiological processes such as tumour suppression, wound healing and embryonic development, whilst paradoxically they can contribute to ageing, cancer and age-related disease.
As such, the field of cellular senescence represents a multidisiplinary research topic.
For review articles on cell senescence click HERE
click HERE for past conferences
More senescence conferences...
Cell Senescence News
Paper of the Month
Cun Wang, Serena Vegna, Haojie Jin, Bente Benedict, Cor Lieftink, Christel Ramirez, Rodrigo Leite de Oliveira, Ben Morris, Jules Gadiot, Wei Wang, Aimée du Chatinier, Liqin Wang, Dongmei Gao, Bastiaan Evers, Guangzhi Jin, Zheng Xue, Arnout Schepers, Fleur Jochems, Antonio Mulero Sanchez, Sara Mainardi, Hein te Riele, Roderick L. Beijersbergen, Wenxin Qin1, Leila Akkari & René Bernards
Liver cancer remains difficult to treat, owing to a paucity of drugs that target critical dependencies; broad-spectrum kinase inhibitors such as sorafenib provide only a modest benefit to patients with hepatocellular carcinoma. The induction of senescence may represent a strategy for the treatment of cancer, especially when combined with a second drug that selectively eliminates senescent cancer cells (senolysis)4,5 . Here, using a kinome-focused genetic screen, we show that pharmacological inhibition of the DNA-replication kinase CDC7 induces senescence selectively in liver cancer cells with mutations in TP53. A follow-up chemical screen identified the antidepressant sertraline as an agent that kills hepatocellular carcinoma cells that have been rendered senescent by inhibition of CDC7. Sertraline suppressed mTOR signalling, and selective drugs that target this pathway were highly effective in causing the apoptotic cell death of hepatocellular carcinoma cells treated with a CDC7 inhibitor. The feedback reactivation of mTOR signalling after its inhibition6 is blocked in cells that have been treated with a CDC7 inhibitor, which leads to the sustained inhibition of mTOR and cell death. Using multiple in vivo mouse models of liver cancer, we show that treatment with combined inhibition of of CDC7 and mTOR results in a marked reduction of tumour growth. Our data indicate that exploiting an induced vulnerability could be an effective treatment for liver cancer.
Institute for Research
and Biomedicine, Barcelona,
Ludwig Institute for Cancer Research, Oxford, UK
Steering Committee Members
University Hospital Tübingen,
Health Research Institute of Santiago de Compostela,
Santiago de Compostela, Spain
Charité-Universitätsmedizin Berlin (CVK), and Max-Delbrück-Center for Molecular Medicine, Berlin, German
University of London,
University of Groningen,
Royal Melbourne Hospital
University of Melbourne,
Département de biochimie
Faculté de Médecine
Université de Montréal
Live Longer, Live Well
Telomeres and Cell Senescence
Researchers Extend Lifespan by as Much as 35 Percent in Mice
How to join ICSA?
The cost of registration for one year of ICSA membership is:
Standard - 50€
Student/Postdoc - 25€
To become a member, follow this link.
*** REGISTER NOW FOR 2020 ***