ICSA2020 #icsa2020osaka

http://www.icsa2020-osaka.jp

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December 12-15, 2021

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Members Featured Articles

The Cancer SENESCopedia:

A delineation of cancer cell senescence

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Fleur Jochems, Bram Thijssen, Giulia De Conti, Robin Jansen, Ziva Pogacar, Kelvin Groot, Liqin Wang, Arnout Schepers, Cun Wang, Haojie Jin, Roderick L.Beijersbergen, Rodrigo Leite de Oliveira, Lodewyk F.A. Wessels, René Bernards

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Cellular senescence is characterized as a stable proliferation arrest that can be triggered by multiple stresses. Most knowledge about senescent cells is obtained from studies in primary cells. However, senescence features may be different in cancer cells, since the pathways that are involved in senescence induction are often deregulated in cancer. We report here a comprehensive analysis of the transcriptome and senolytic responses in a panel of 13 cancer cell lines rendered senescent by two distinct compounds. We show that in cancer cells, the response to senolytic agents and the composition of the senescence-associated secretory phenotype are more influenced by the cell of origin than by the senescence trigger. Using machine learning, we establish the SENCAN gene expression classifier for the detection of senescence in cancer cell samples. The expression profiles and senescence classifier are available as an interactive online Cancer SENESCopedia.

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More ICSA members featured articles here

Paper of the Month

Cellular senescence inhibits renal regeneration after injury in mice, with senolytic treatment promoting repair

Katie J. Mylonas, Eoin D. O'Sullivan, Duncan Humphries, David P. Baird, Marie-Helena Docherty, Sarah A. Neely, Paul J. Krimpen, Fortanette Melk, Roland Schmitt, Sofia Ferreira-Gonzalez, Stuart J. Forbes, Jeremy Hughes and David A. Ferenbach

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The ability of the kidney to regenerate successfully after injury is lost with advancing age, chronic kidney disease, and after irradiation. The factors responsible for this reduced regenerative capacity remain incompletely understood, with increasing interest in a potential role for cellular senescence in determining outcomes after injury. Here, we demonstrated correlations between senescent cell load and functional loss in human aging and chronic kidney diseases including radiation nephropathy. We dissected the causative role of senescence in the augmented fibrosis occurring after injury in aged and irradiated murine kidneys. In vitro studies on human proximal tubular epithelial cells and in vivo mouse studies demonstrated that senescent renal epithelial cells produced multiple components of the senescence-associated secretory phenotype including transforming growth factor β1, induced fibrosis, and inhibited tubular proliferative capacity after injury. Treatment of aged and irradiated mice with the B cell lymphoma 2/w/xL inhibitor ABT-263 reduced senescent cell numbers and restored a regenerative phenotype in the kidneys with increased tubular proliferation, improved function, and reduced fibrosis after subsequent ischemia-reperfusion injury. Senescent cells are key determinants of renal regenerative capacity in mice and represent emerging treatment targets to protect aging and vulnerable kidneys in man.

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