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Nuclear inositide signaling in myelodysplastic syndromes
Author(s) -
Follo Matilde Y.,
Mongiorgi Sara,
Finelli Carlo,
Clissa Cristina,
Ramazzotti Giulia,
Fiume Roberta,
Faenza Irene,
Manzoli Lucia,
Martelli Alberto M.,
Cocco Lucio
Publication year - 2010
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.22483
Subject(s) - myeloid leukemia , signal transduction , haematopoiesis , biology , myelodysplastic syndromes , bone marrow , myeloid , cancer research , leukemia , stem cell , cell cycle , hematopoietic stem cell , microbiology and biotechnology , cell , immunology , genetics
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.