Dialogue calcique et Sénescence
David Bernard
« Senescence Escape Mechanisms » lab -
Tumoral Escape Department
-β
ββ
βgalactosidase activity at pH6 (SA b Gal)
(Dimri et al, PNAS, 1995)
-Morphological alterations
(Hayflick et al, Exp Cell Res,1965)
young
-Secretory phenotype (SASP)
(Coppe et al, PLos Biol, 2008) n
s
-A stable form of cell cycle arrest
(Hayflick et al, Exp Cell Res, 1965) senescence
What is cellular senescence ?
-where it occurs : in normal (replicative and premature) but
also in cancer cells (premature)
-how is it induced: by various stresses (short telomeres,
oncogenes,oxidative stress, genotoxic drugs…)
Senescence: a stable proliferation arrest
-how is it recognized : SAbGal activity, strongly released
cytokines (SASP), may display nuclear heterochromatin dots
(SAHF) and others markers have been proposed
Physiopathological functions of cellular senescence
Senescence
Timely:
-tumor suppressive
-embryonic development
-wound healing
Chronic:
-tumor promoter
-progeria/aging
-aging related deseases
Physiopathological functions of cellular senescence
Senescence
Timely:
-tumor suppressive
-embryonic development
-wound healing
Chronic:
-tumor promoter
-progeria/aging
-aging related deseases
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