Peter P. Ruvolo

TL;DR: ABT-737 effectively kills acute myeloid leukemia blast, progenitor, and stem cells without affecting normal hematopoietic cells, suggesting that ABT- 737 could be a highly effective antileukemia agent when the mechanisms of resistance identified here are considered.

TL;DR: It is demonstrated that acute myeloid leukemia cell lines, primary patient samples, and murine primary xenografts are very sensitive to treatment with the selective BCL-2 antagonist ABT-199, and mitochondrial studies using BH3 profiling demonstrate activity at the mitochondrion that correlates well with cytotoxicity, supporting an on-target mitochondrial mechanism of action.

TL;DR: The findings indicate that simple expression of Bcl2 may not be enough to functionally protect cells from apoptosis, and the regulatory role for phosphorylation is focused on and its potential clinical ramifications are discussed.

TL;DR: Findings indicate a novel role for JNK1 as a SAK and may explain, at least in part, how functional phosphorylation of Bc12 can occur in the absence of growth factor.

TL;DR: It is shown that aurintricarboxylic acid (ATA), a nonpeptide activator of cellular MEK/mitogen-activated protein kinase (MAPK) kinase, can induce Ser-70 phosphorylation of Bcl2 and support survival of cells expressing wild-type but not the phosphorylations-incompetent S70A mutant B cl2, suggesting a role for the ERK1/2 kinases as SRKs.