The 41 patients with the t(1;19) had a comparable event-free survival to that of the 694
patients with other B-cell precursor ALL (P = 0.63; 84.2 +/- 7.1% (s.e.) vs 84.0 +/- 1.8% at 5 years). However, patients with the t(1; 19) had a lower cumulative incidence of any hematological relapse (P = 0.06; 0 vs 8.3 +/- 1.2% at 5 years) but a significantly higher incidence of central nervous system (CNS) relapse (P < 0.001; 9.0 +/- 5.1% vs 1.0 +/- 0.4% at 5 years). In a multivariate analysis, the t(1; 19) was an independent risk factor for isolated CNS relapse. These data suggest that with contemporary treatment, patients with the t(1; 19) and TCF3/PBX1 fusion have a favorable overall outcome but increased risk of CNS relapse. Leukemia (2009) 23, 1406-1409; doi:10.1038/leu.2009.42; published online 12 March 2009″
“Anxiety disorders, depression and animal models of selleck chemicals vulnerability to a depression-like syndrome have been associated with dysregulation of brain serotonergic systems. These effects could result from genetic influences, adverse early life experiences (ELE), or acute stressful life events, all of which can alter serotonergic neurotransmission and have been implicated in determining vulnerability to neuropsychiatric disorders. Selleckchem Alvocidib To evaluate the effects of ELE, adverse experiences during adulthood, and potential interactions
between these factors on neuronal tryptophan hydroxylase 2 (tph2) mRNA expression, we
investigated in rats the effects of maternal separation (MS)(separation from the dam for 180 min/day from postnatal day 2-14; MS180, a model of vulnerability to a depression-like syndrome), neonatal handling (separation from the dam for 15 min/day from postnatal day 2-14; MS15, a model of decreased stress sensitivity), or normal animal facility rearing (AFR) control conditions, with or without subsequent exposure to adult social defeat, on tph2 mRNA expression in the dorsal raphe nucleus (DR). Among rats exposed to social defeat, MS180 rats had increased tph2 mRNA expression in the DR, while MS15 rats had decreased tph2 mRNA expression see more compared to AFR rats. Social defeat increased tph2 mRNA expression, but only in MS180 rats and only in the “”lateral wings”" of the DR, a subdivision of the DR that is part of a sympathomotor command center. Overall, these data demonstrate that ELE and stressful experience during adulthood interact to determine tph2 mRNA expression. These changes in tph2 mRNA expression represent a potential mechanism through which adverse ELEs and stressful life experiences during adulthood may interact to increase vulnerability to stress-related psychiatric disease. (C) 2009 IBRO. Published by Elsevier Ltd. All rights reserved.