Microsatellite instability induced mutations in DNA repair genes CtIP and MRE11 confer hypersensitivity to poly (ADP-ribose) polymerase inhibitors in myeloid malignancies.

Inactivation of the DNA mismatch repair pathway manifests as microsatellite instability, an accumulation of mutations that drives carcinogenesis. Here, we determined whether microsatellite instability in acute myeloid leukemia and myelodysplastic syndrome correlated with chromosomal instability and poly (ADP-ribose) polymerase (PARP) inhibitor sensitivity through disruption of DNA repair function. Acute myeloid leukemia cell lines (n=12) and primary cell samples (n=18), and bone marrow mononuclear cells from high-risk myelodysplastic syndrome patients (n=63) were profiled for microsatellite instability using fluorescent fragment polymerase chain reaction.

Co-localization of PRiMA with acetylcholinesterase in cholinergic neurons of rat brain: an immunocytochemical study.

In the central nervous system, acetylcholinesterase (AChE) is present in a tetrameric form that is anchored to membranes via a proline-rich membrane anchor (PRiMA). Previously it has been found that principal cholinergic neurons in the brain express high concentrations of AChE enzymic activity at their neuronal membranes. The aim of this study was to use immunocytochemical methods to determine the distribution of PRiMA in these neurons in the rat brain.