FER is required for cell cycle transitions, whereas FES seems necessary for cell survival. We concluded that FES and FER

kinases mediate essential non-redundant functions downstream of FLT3-ITD. Leukemia (2010) 24, 721-728; doi: 10.1038/leu.2009.301; published online 28 January 2010″
“There is an abundant literature on the adverse effects of solvents on the neurobehavioral performance, Selleckchem JSH-23 higher brain functions, and chronic solvent-induced encephalopathy. However, the occurrence of solvent-related schizophrenia is rare, with few reports on the link between solvent exposure and schizophrenia. Here, we report on a patient with schizophrenia, presenting after a sustained period of 6 months of everyday exposure to neurotoxic solvents in an unprotected occupational setting in Haifa, Israel. In light of the similarity of symptoms of schizophrenia and chronic solvent encephalopathy, we call for further epidemiologic YM155 studies to examine the potential contribution of solvent exposure to the etiology

and evolution of schizophrenia in selected cases. This case study and review of relevant literature underscores the importance of obtaining detailed histories on occupational exposures to search for agents which can trigger psychotic episodes. In the meantime, policies to prevent such exposures at the source can be expected to contribute to the prevention of a non-trivial proportion of neurotoxic diseases, including, possibly, schizophrenia in worker populations. (C) 2010 Elsevier Inc. All rights reserved.”
“Retinoic acid (RA) relieves the

maturation block in t(15:17) acute promyelocytic leukemia (APL), leading to granulocytic differentiation. However, RA treatment alone invariably results in RA resistance, both in vivo and in vitro. RA-resistant cell lines have been shown Alisertib cell line to serve as useful models for elucidation of mechanisms of resistance. Previously, we identified topoisomerase II beta (TOP2B) as a novel mediator of RA-resistance in APL cell lines. In this study, we show that both TOP2B protein stability and activity are regulated by a member of the protein kinase C (PRKC) family, PRKC delta (PRKCD). Co-treatment with a pharmacologic inhibitor of PRKCD and RA resulted in the induction of an RA responsive reporter construct, as well as the endogenous RA target genes, CEBPE, CYP26A1 and RIG-I. Furthermore, the co-treatment overcame the differentiation block in RA-resistant cells, as assessed by morphological analysis, restoration of promyelocytic leukemia nuclear bodies, induction of CD11c cell surface expression and an increase in nitro-blue-tetrazolium reduction. Cumulatively, our data suggest a model whereby inhibition of PRKCD decreases TOP2B protein levels, leading to a loss of TOP2B-mediated repressive effects on RA-induced transcription and granulocytic differentiation. Leukemia (2010) 24, 729-739; doi: 10.1038/leu.2010.