Inositide-dependent signaling pathways as new therapeutic targets in myelodysplastic syndromes
Cited 0 times inCited 0 times in
- Inositide-dependent signaling pathways as new therapeutic targets in myelodysplastic syndromes
- Mongiorgi, Sara; Finelli, Carlo; Yang, Young Ryoul; Clissa, Cristina; McCubrey, James A.; Billi , Anna Maria; Manzoli, Lucia; Suh, Pann-Ghill; Cocco, Lucio; Follo, Marilde Y.
- Myelodysplastic syndromes; nuclear inositides; PI-PLCbeta1; PI-PLCgamma1; PI3K/Akt/mTOR
- Issue Date
- INFORMA HEALTHCARE
- EXPERT OPINION ON THERAPEUTIC TARGETS, v.20, no.6, pp.677 - 687
- Introduction: Nuclear inositide signaling pathways specifically regulate cell proliferation and differentiation. Interestingly, the modulation of nuclear inositides in hematological malignancies can differentially affect erythropoiesis or myelopoiesis. This is particularly important in patients with myelodysplastic syndromes (MDS), who show both defective erythroid and myeloid differentiation, as well as an increased risk of evolution into acute myeloid leukemia (AML). Areas covered: This review focuses on the structure and function of specific nuclear inositide enzymes, whose impairment could be linked with disease pathogenesis and cancer. The authors, stemming from literature and published data, discuss and describe the role of nuclear inositides, focusing on specific enzymes and demonstrating that targeting these molecules could be important to develop innovative therapeutic approaches, with particular reference to MDS treatment. Expert opinion: Demethylating therapy, alone or in combination with other drugs, is the most common and current therapy for MDS patients. Nuclear inositide signaling molecules have been demonstrated to be important in hematopoietic differentiation and are promising new targets for developing a personalized MDS therapy. Indeed, these enzymes can be ideal targets for drug design and their modulation can have several important downstream effects to regulate MDS pathogenesis and prevent MDS progression to AML.
- ; Go to Link
Appears in Collections:
- SLS_Journal Papers
- Files in This Item:
- There are no files associated with this item.
can give you direct access to the published full text of this article. (UNISTARs only)
Show full item record
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.