Nuclear inositide signaling in myelodysplastic syndromes |
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| Authors: | Matilde Y. Follo Sara Mongiorgi Carlo Finelli Cristina Clissa Giulia Ramazzotti Roberta Fiume Irene Faenza Lucia Manzoli Alberto M. Martelli Lucio Cocco |
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| Affiliation: | 1. Cellular Signaling Laboratory, Department of Human Anatomical Sciences, University of Bologna, via Irnerio 48, 40126 Bologna, Italy;2. Institute of Hematology and Medical Oncology “L. e A. Seràgnoli”, University of Bologna, via Massarenti 9, 40138, Bologna, Italy;3. Istituto per i Trapianti d'Organo e l'Immunocitologia, Consiglio Nazionale delle Ricerche, Sezione di Bologna c/o I.O.R., Via di Barbiano 1/10, 40136 Bologna, Italy |
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| Abstract: | Myelodysplastic syndromes (MDS) are defined as clonal hematopoietic stem‐cell disorders characterized by ineffective hematopoiesis in one or more of the lineages of the bone marrow. Although distinct morphologic subgroups exist, the natural history of MDS is progression to acute myeloid leukemia (AML). However, the molecular the mechanisms the underlying MDS evolution to AML are not completely understood. Inositides are key cellular second messengers with well‐established roles in signal transduction pathways, and nuclear metabolism elicited by phosphoinositide‐specific phospholipase C (PI‐PLC) β1 and Akt plays an important role in the control of the balance between cell cycle progression and apoptosis in both normal and pathologic conditions. Recent findings evidenced the role played by nuclear lipid signaling pathways, which could become promising therapeutic targets in MDS. This review will provide a concise and updated revision of the state of art on this topic. J. Cell. Biochem. 109: 1065–1071, 2010. © 2010 Wiley‐Liss, Inc. |
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| Keywords: | signal transduction PI‐PLCbeta1 myelodysplastic syndromes Akt nucleus |
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