Acute lymphoblastic leukemia (ALL) https://greenmedinfo.com/category/keywords/Acute%20lymphoblastic%20leukemia%20%28ALL%29 en Fasting selectively blocks development of acute lymphoblastic leukemia. https://greenmedinfo.com/article/fasting-selectively-blocks-development-acute-lymphoblastic-leukemia n/a PMID:  Nat Med. 2017 Jan ;23(1):79-90. Epub 2016 Dec 12. PMID: 27941793 Abstract Title:  Fasting selectively blocks development of acute lymphoblastic leukemia via leptin-receptor upregulation. Abstract:  New therapeutic approaches are needed to treat leukemia effectively. Dietary restriction regimens, including fasting, have been considered for the prevention and treatment of certain solid tumor types. However, whether and how dietary restriction affects hematopoietic malignancies is unknown. Here we report that fasting alone robustly inhibits the initiation and reverses the leukemic progression of both B cell and T cell acute lymphoblastic leukemia (B-ALL and T-ALL, respectively), but not acute myeloid leukemia (AML), in mouse models of these tumors. Mechanistically, we found that attenuated leptin-receptor (LEPR) expression is essential for the development and maintenance of ALL, and that fasting inhibits ALL development by upregulation of LEPR and its downstream signaling through the protein PR/SET domain 1 (PRDM1). The expression of LEPR signaling-related genes correlated with the prognosis of pediatric patients with pre-B-ALL, and fasting effectively inhibited B-ALL growth in a human xenograft model. Our results indicate that the effects of fasting on tumor growth are cancer-type dependent, and they suggest new avenues for the development of treatment strategies for leukemia. https://greenmedinfo.com/article/fasting-selectively-blocks-development-acute-lymphoblastic-leukemia#comments Acute lymphoblastic leukemia (ALL) Acute T cell Leukemias Antiproliferative Chemopreventive Fasting/Caloric Restriction Acute lymphoblastic leukemia (ALL) Acute T cell Leukemias Antiproliferative Chemopreventive Fasting/Caloric Restriction Gene Exprsession Regulation Selective Antiproliferation Animal Study Tue, 17 Jan 2017 03:57:26 +0000 greenmedinfo 142072 at https://greenmedinfo.com Forced inhibition of PDE1A expression might be a new therapeutic strategy for the management of acute lymphoblastic leukemia. https://greenmedinfo.com/article/forced-inhibition-pde1a-expression-might-be-new-therapeutic-strategy-managemen n/a PMID:  Cell Signal. 2011 Jan ;23(1):152-60. Epub 2010 Aug 31. PMID: 20807569 Abstract Title:  Down-regulation of cyclic nucleotide phosphodiesterase PDE1A is the key event of p73 and UHRF1 deregulation in thymoquinone-induced acute lymphoblastic leukemia cell apoptosis. Abstract:  Thymoquinone (TQ), the active principle of Nigella sativa black seeds, has anti-proliferative properties on numerous cancer cell types. Others and we have previously reported that TQ acts as agent that triggers cell cycle arrest and apoptosis through either a p53- or p73-dependent pathway. However, the immediate targets recruited upon TQ-induced cytotoxicity have not yet been clearly identified. We therefore asked whether cyclic nucleotide phosphodiesterases (PDEs) could be involved in TQ-triggered pro-apoptotic reactivity; PDEs are regulators of intracellular levels of cyclic nucleotides and therefore can modulate cAMP and cGMP-dependent cell death pathways. Our results showed that TQ specifically repressed PDE1A expression in the acute lymphoblastic leukemia Jurkat cell line. This effect is concomitant with the previously described sequential deregulation of the expression of the tumor suppressor protein p73 and the epigenetic integrator UHRF1 (Ubiquitin-like, PHD Ring Finger 1). Interestingly, RNA-interference knock-down of PDE1A expression as well as decreased PDE1A expression induced growth inhibition of Jurkat cells, cell cycle arrest and apoptosis through an activation of p73 and a repression of UHRF1. Conversely, PDE1A re-expression counteracted the cellular pro-apoptotic effects of TQ in association with a p73 repression and UHRF1 re-expression. Altogether, our results show that TQ induced an initial down-regulation of PDE1A with a subsequent down-regulation of UHRF1 via a p73-dependent mechanism. This study further proposes that PDE1A might be involved in the epigenetic code inheritance by regulating, via p73, the epigenetic integrator UHRF1. Our findings also suggest that a forced inhibition of PDE1A expression might be a new therapeutic strategy for the management of acute lymphoblastic leukemia. https://greenmedinfo.com/article/forced-inhibition-pde1a-expression-might-be-new-therapeutic-strategy-managemen#comments Acute lymphoblastic leukemia (ALL) Thymoquinone Antineoplastic Agents Apoptotic Acute lymphoblastic leukemia (ALL) Antineoplastic Agents Apoptotic thymoquinone In Vitro Study Fri, 28 Apr 2017 20:00:03 +0000 greenmedinfo 146989 at https://greenmedinfo.com