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Jean-Luc Perfettini

Researcher at Institut Gustave Roussy

Publications -  60
Citations -  7329

Jean-Luc Perfettini is an academic researcher from Institut Gustave Roussy. The author has contributed to research in topics: Programmed cell death & Apoptosis. The author has an hindex of 28, co-authored 56 publications receiving 6598 citations. Previous affiliations of Jean-Luc Perfettini include French Institute of Health and Medical Research & University of Paris-Sud.

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Inhibition of macroautophagy triggers apoptosis.

TL;DR: Data indicate that autophagy may be cytoprotective, at least under conditions of nutrient depletion, and point to an important cross talk between type 1 and type 2 cell death pathways.
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Activation of the NLRP3 inflammasome in dendritic cells induces IL-1β–dependent adaptive immunity against tumors

TL;DR: It is shown that dying tumor cells release ATP, which then acts on P2X7 purinergic receptors from DCs and triggers the NOD-like receptor family, pyrin domain containing-3 protein (NLRP3)-dependent caspase-1 activation complex ('inflammasome'), allowing for the secretion of interleukin-1 β (IL-1β).
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Cell death by mitotic catastrophe : a molecular definition

TL;DR: It is proposed that mitotic catastrophe results from a combination of deficient cell-cycle checkpoints and cellular damage and failure to arrest the cell cycle before or at mitosis triggers an attempt of aberrant chromosome segregation, which culminates in the activation of the apoptotic default pathway and cellular demise.
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Mitotic catastrophe constitutes a special case of apoptosis whose suppression entails aneuploidy

TL;DR: A molecular pathway through which DNA damage, failure to arrest the cell cycle and inhibition of apoptosis can favor the occurrence of cytogenetic abnormalities that are likely to participate in oncogenesis is delineated.
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Chemotherapy induces ATP release from tumor cells.

TL;DR: It is described that multiple distinct anticancer drugs reduce the intracellular concentration of ATP before and during the manifestation of apoptotic characteristics such as the dissipation of the mitochondrial transmembrane potential and the exposure of phosphatidylserine residues on the plasma membrane.