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Suh, Pann-Ghill
BioSignal Network Lab (BSN)
Research Interests
  • Signal transduction, cancer, metabolism, phospholipase C

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Inositide-dependent signaling pathways as new therapeutic targets in myelodysplastic syndromes

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Title
Inositide-dependent signaling pathways as new therapeutic targets in myelodysplastic syndromes
Author
Mongiorgi, SaraFinelli, CarloYang, Young RyoulClissa, CristinaMcCubrey, James A.Billi , Anna MariaManzoli, LuciaSuh, Pann-GhillCocco, LucioFollo, Marilde Y.
Issue Date
2016-06
Publisher
INFORMA HEALTHCARE
Citation
EXPERT OPINION ON THERAPEUTIC TARGETS, v.20, no.6, pp.677 - 687
Abstract
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.
URI
https://scholarworks.unist.ac.kr/handle/201301/18014
URL
http://www.tandfonline.com/doi/abs/10.1517/14728222.2016.1125885?journalCode=iett20
DOI
10.1517/14728222.2016.1125885
ISSN
1472-8222
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BIO_Journal Papers
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