Synergistic induction of PI-PLC²1 signaling by azacitidine and valproic acid in high-risk myelodysplastic syndromes. (Articolo in rivista)

Type
Label
  • Synergistic induction of PI-PLC²1 signaling by azacitidine and valproic acid in high-risk myelodysplastic syndromes. (Articolo in rivista) (literal)
Anno
  • 2011-01-01T00:00:00+01:00 (literal)
Alternative label
  • Follo MY, Finelli C, Mongiorgi S, Clissa C, Chiarini F, Ramazzotti G, Paolini S, Martinelli G, Martelli AM, Cocco L. (2011)
    Synergistic induction of PI-PLC²1 signaling by azacitidine and valproic acid in high-risk myelodysplastic syndromes.
    in Leukemia
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Follo MY, Finelli C, Mongiorgi S, Clissa C, Chiarini F, Ramazzotti G, Paolini S, Martinelli G, Martelli AM, Cocco L. (literal)
Pagina inizio
  • 271 (literal)
Pagina fine
  • 280 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 25 (literal)
Rivista
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Department of Human Anatomical Sciences, Cellular Signalling Laboratory, University of Bologna, Bologna, Italy; Institute of Hematology and Medical Oncology ‘L. e A. Seragnoli’, University of Bologna, Bologna, Italy; Istituto per i Trapianti d’Organo e l’Immunocitologia del C.N.R., Sezione di Bologna c/o I.O.R., Bologna, Italy (literal)
Titolo
  • Synergistic induction of PI-PLC²1 signaling by azacitidine and valproic acid in high-risk myelodysplastic syndromes. (literal)
Abstract
  • The association between azacitidine (AZA) and valproic acid (VPA) has shown high response rates in high-risk myelodysplastic syndromes (MDS) cases with unfavorable prognosis. However, little is known about the molecular mechanisms underlying this therapy, and molecular markers useful to monitor the disease and the effect of the treatment are needed. Phosphoinositide-phospholipase C (PI-PLC) ²1 is involved in both genetic and epigenetic mechanisms of MDS progression to acute myeloid leukemia. Indeed, AZA as a single agent was able to induce PI-PLC²1 expression, therefore providing a promising new tool in the evaluation of response to demethylating therapies. In this study, we assessed the efficacy of the combination of AZA and VPA on inducing PI-PLC²1 expression in high-risk MDS patients. Furthermore, we observed an increase in Cyclin D3 expression, a downstream target of PI-PLC²1 signaling, therefore suggesting a potential combined activity of AZA and VPA in high-risk MDS in activating PI-PLC²1 signaling, thus affecting cell proliferation and differentiation. Taken together, our findings might open up new lines of investigations aiming at evaluating the role of the activation of PI-PLC²1 signaling in the epigenetic therapy, which may also lead to the identification of innovative targets for the epigenetic therapy of high-risk MDS. (literal)
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