Hossein A. Hamed

TL;DR: This review discusses how autophagy, a process in which de novo formed membrane enclosed vesicles engulf and consume cellular components, has been shown to engage in complex interplay with apoptosis, and the boundary between Type I and II cell death is not completely clear.

TL;DR: In this article, low doses of sorafenib and vorinostat interact in a synergistic fashion to kill carcinoma cells by activating CD95, and this drug combination is entering phase I trials.

TL;DR: The results provide the first evidence for a mechanism by which mitoStat3 contributes to tumorigenesis and suggest a novel role for mitostat3 in regulation of ROS concentrations through its action on the ETC.

TL;DR: Combined exposure of epithelial tumor cell types to sorafenib and vorinostat diminishes expression of multiple antiapoptotic proteins and promotes activation of the CD95 extrinsic apoptotic and the lysosomal protease pathways, and that suppression of c-FLIP-s expression represents a critical event in transduction of the proapoptosis signals from CD95 to promote mitochondrial dysfunction and death.

TL;DR: The data suggest that premexetred and sorafenib act synergistically to enhance tumor killing via the promotion of a toxic form of autophagy that leads to activation of the intrinsic apoptosis pathway, and predict that combination treatment represents a future therapeutic option in the treatment of solid tumors.