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 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.
Follo MY, Mongiorgi S, Finelli C, Clissa C, Ramazzotti G, Fiume R, et al. (2010). Nuclear inositide signaling in myelodysplastic syndromes. JOURNAL OF CELLULAR BIOCHEMISTRY, 109 (6), 1065-1071 [10.1002/jcb.22483].
Nuclear inositide signaling in myelodysplastic syndromes.
FOLLO, MATILDE YUNG;MONGIORGI, SARA;FINELLI, CARLO;CLISSA, CRISTINA;RAMAZZOTTI, GIULIA;FIUME, ROBERTA;FAENZA, IRENE;MANZOLI, LUCIA;MARTELLI, ALBERTO MARIA;COCCO, LUCIO ILDEBRANDO
2010
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 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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
