Seshagiri Duvvuri

TL;DR: It is demonstrated that pharmacologic inhibition of FAO with etomoxir or ranolazine inhibited proliferation and sensitized human leukemia cells to apoptosis induction by ABT-737, and evidence suggesting that FAO regulates the activity of Bak-dependent mitochondrial permeability transition is generated.

TL;DR: Data suggest that CRM1 exerts an antiapoptotic function and is highly prognostic in AML, and a novel combinatorial approach is proposed aimed at maximal activation of p53-mediated apoptosis by concomitant MDM2 andCRM1 inhibition.

TL;DR: R reverse phase protein analysis of 230 proteins in 511 AML patient samples revealed a strong correlation of B55α with a number of proteins including MYC, PKC α, and SRC, and suppression in OCI-AML3 cells by shRNA demonstrated that the B subunit is a PKCα phosphatase.

TL;DR: The role of p53 in sensitivity of CLL cells to BCL‐2 inhibition has not been extensively investigated and the small‐molecule B CL‐2 inhibitor ABT‐737 induces apoptosis in a BAX‐dependent and BCL-2 homologous antagonist‐killer (BAK)‐dependent manner.

TL;DR: Autophagy induction in acute leukemia by Nutlin 3a, a first-in-class MDM2 inhibitor, appears to be pro-apoptotic as pharmacological (bafilomycin) or genetic inhibition of autophagy impairs apoptosis induced by Nutlins 3a.