Sorafenib and HDAC inhibitors synergize to kill CNS tumor cells

HDAC inhibitors enhance the lethality of low dose salinomycin in parental and stem-like GBM cells

“…Further detailed studies will be required to fully understand the mechanisms by which valproate interacts with the salinomycin-induced autophagy process. Prior studies by this group have shown that HDAC inhibitors can enhance the expression of toxic BH3 domain proteins as well as the death receptor CD95 and its ligand FAS-L. 21,22 We have also shown that HDAC inhibitors can facilitate the tyrosine phosphorylation of CD95 thereby promoting its ligand independent activation. 23 The mechanisms by which CD95 tyrosine phosphorylation can be increased include elevated levels of ROS, which is in agreement with our data showing that drug combination killing correlated with increased ROS and that quenching of ROS was protective.…”

“…Antibody reagents, other kinase inhibitors, caspase inhibitors cell culture reagents, and non-commercial recombinant adenoviruses have been previously described. [21][22][23][25][26][27][28] …”

The multi-hit hypothesis in basal-like breast cancer

“…Genes most commonly associated with the process of oncogenesis include: p53 inactivating mutation; hDM2 overexpression; p16 reduced expression; K-/H-RAS activating mutation; PTEN inactivating mutation/deletion; EGFR activating mutation and overexpression; retinoblastoma inactivating mutation and deletion; Cyclin proteins overexpression; CD95 reduced expression; protective BCL-2 proteins overexpression; to name but just a few of such molecules 1 - 5 . That the minimally required specific proteins for oncogenesis are not known for many specific tumor types remains a challenge for the rational design of molecular targeted therapies.…”

The Epigenetics of Medulloblastoma

“…For instance, Lee et al demonstrated that curcumin reduces medulloblastoma cell growth in vitro and in vivo via HDAC regulation and tubulin modification [17]. Similarly, combining the HDAC inhibitor valproic acid with the kinase inhibitor sorafenib, which targets Raf, VEGF (vascular endothelial growth factor), and PDGF (platelet-endothelial growth factor) receptors [40], induced radiosensitization of medulloblastoma cells [41]. Further, tubulin acetylation was increased after curcumin treatment.…”