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

 

ICSA2020 #icsa2020osaka

ICSA2020 in Osaka[18575].jpg

**Postponed**

Please save the new dates:

June 7-10, 2021

click HERE for past conferences

More senescence conferences...

COMPARATIVE BIOLOGY OF AGING

15-19 Jun 2020 Roscoff (France)

***Postponed***

 

Cell Senescence News

 
ICSA Header.png

Members Featured Articles

kisspng-pdf-computer-icons-download-pdf-
Senescence Reprogramming by TIMP1 Deficiency Promotes Prostate Cancer Metastasis

 

Ilaria Guccini, Ajinkya Revandkar, Mariantonietta D'Ambrosio, Manuel Colucci, Emiliano Pasquini, Simone Mosole, Martina Troiani, Daniela Brina, Raheleh Sheibani-Tezerji, Angela Rita Elia, Andrea Rinaldi, Nicolò Pernigoni, Jan Hendrik Rüschoff, Susanne Dettwiler, Angelo M. De Marzo, Emmanuel S. Antonarakis, Costanza Borrelli, Andreas E. Moor, Ramon Garcia-Escudero, Abdullah Alajati, Giuseppe Attanasio, Marco Losa, Holger Moch, Peter Wild, Gerda Egger, Andrea Alimonti

Metastases account for most cancer-related deaths, yet the mechanisms underlying metastatic spread remain poorly understood. Recent evidence demonstrates that senescent cells, while initially restricting tumorigenesis, can induce tumor progression. Here, we identify the metalloproteinase inhibitor TIMP1 as a molecular switch that determines the effects of senescence in prostate cancer. Senescence driven either by PTEN deficiency or chemotherapy limits the progression of prostate cancer in mice. TIMP1 deletion allows senescence to promote metastasis, and elimination of senescent cells with a senolytic BCL-2 inhibitor impairs metastasis. Mechanistically, TIMP1 loss reprograms the senescence-associated secretory phenotype (SASP) of senescent tumor cells through activation of matrix metalloproteinases (MMPs). Loss of PTEN and TIMP1 in prostate cancer is frequent and correlates with resistance to docetaxel and worst clinical outcomes in patients treated in an adjuvant setting. Altogether, these findings provide insights into the dual roles of tumor-associated senescence and can potentially impact the treatment of prostate cancer.

More ICSA members featured articles here

https___cdn.evbuc.com_images_87977931_39

Featured Articles

Systemic overexpression of C-C motif chemokine ligand 2 promotes metabolic dysregulation and premature death in mice with accelerated aging

 

Fedra Luciano-Mateo, Noemí Cabré, Gerard Baiges-Gaya, Salvador Fernández-Arroyo, Anna Hernández-Aguilera, Elisabet Rodríguez-Tomàs, Meritxell Arenas, Jordi Camps, Javier A Menéndez, Jorge Joven

Injection of tissues with senescent cells induces changes that mimic aging, and this process is delayed in mice engineered to eliminate senescent cells, which secrete proinflammatory cytokines, including C-C motif chemokine ligand 2 (Ccl2). Circulating levels of Ccl2 correlate with age, but the impact of Ccl2 on tissue homeostasis has not been established. We generated an experimental model by crossbreeding mice overexpressing Ccl2 with progeroid mice bearing a mutation in the lamin A (Lmna) gene. Wild-type animals and progeroid mice that do not overexpress Ccl2 were used as controls. Ccl2 overexpression decreased the lifespan of the progeroid mice and induced the dysregulation of glycolysis, the citric acid cycle and one-carbon metabolism in skeletal muscle, driving dynamic changes in energy metabolism and DNA methylation. This impact on cellular bioenergetics was associated with mitochondrial alterations and affected cellular metabolism, autophagy and protein synthesis through AMPK/mTOR pathways. The data revealed the ability of Ccl2 to promote death in mice with accelerated aging, which supports its putative use as a biomarker of an increased senescent cell burden and for the assessment of the efficacy of interventions aimed at extending healthy aging.

kisspng-pdf-computer-icons-download-pdf-

To learn more about young ICSA (yICSA), click here!

 

About ICSA

President

Manuel Serrano, 

Institute for Research

and Biomedicine, Barcelona, 

Spain

Vice-President

Oliver Bischof

Institut Pasteur,

Paris, France

Treasurer

Sushma-Nagaraja Grellscheid, 

Durham University,

Durham, UK

Secretary

Romuald Binet,

 Ludwig Institute for Cancer Research, Oxford, UK

Website Manager

Dominick Burton,

Loughborough

University, UK

Steering Committee Members

Lars Zender

University Hospital Tübingen,

Tübingen, Germany

Manuel Collado,
Health Research Institute of Santiago de Compostela,

Santiago de Compostela, Spain

Cleo Bishop
Senior Lecturer
Blizard Institute

London, UK
 

Clemens Schmitt

Charité-Universitätsmedizin Berlin (CVK), and Max-Delbrück-Center for Molecular Medicine, Berlin, German

Dorothy Bennett 

St George's,

University of London,

UK

Marco Demaria

Faculty of Medical Sciences

University of Groningen,

Netherlands

Andrea Maier

Royal Melbourne Hospital

University of Melbourne,

Australia

Gerardo Ferbeyre 

Département de biochimie
Faculté de Médecine
Université de Montréal

Learn More

Live Longer, Live Well

Telomeres and Cell Senescence

Researchers Extend Lifespan by as Much as 35 Percent in Mice

 
 

ICSA Membership

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 2021 ***

ALREADY A MEMBER?

Access your personal page here.