PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22033492-0 2012 Epigenetic regulation of nuclear PI-PLCbeta1 signaling pathway in low-risk MDS patients during azacitidine treatment. Azacitidine 95-106 phospholipase C beta 1 Homo sapiens 36-44 25977289-0 2015 An increased expression of PI-PLCbeta1 is associated with myeloid differentiation and a longer response to azacitidine in myelodysplastic syndromes. Azacitidine 107-118 phospholipase C beta 1 Homo sapiens 30-38 25977289-4 2015 Overall, 60 patients completed 6 cycles of azacitidine, and for them, a clinical and molecular evaluation was possible: 37 of these patients (62%) showed a specific increase of PI-PLCbeta1 mRNA within the first 3 cycles, which was associated with a longer duration of response and with an increased myeloid differentiation, as evidenced by PI-PLCgamma2 induction and the recruitment of specific myeloid-associated transcription factors to the PI-PLCbeta1 promoter during azacitidine response. Azacitidine 43-54 phospholipase C beta 1 Homo sapiens 180-188 25977289-5 2015 Moreover, the increase of cyclin D3 gene expression throughout all of the therapy showed that PI-PLCbeta1-dependent signaling is indeed activated in azacitidine responder patients. Azacitidine 149-160 phospholipase C beta 1 Homo sapiens 97-105 25977289-6 2015 Taken together, our results show that PI-PLCbeta1 quantification in MDS predicts the response to azacitidine and is associated with an increased myeloid differentiation. Azacitidine 97-108 phospholipase C beta 1 Homo sapiens 41-49 25307310-6 2014 In the last few years, a role for nuclear inositide signalling as a therapeutic target in MDS has been disclosed, in that PI-PLCβ1 increase is associated with azacitidine responsiveness, even when this drug is used in combination with other agents, and Akt is specifically activated in MDS at higher risk of AML evolution. Azacitidine 168-179 phospholipase C beta 1 Homo sapiens 122-128 23596104-14 2013 PI-PLCbeta1 gene expression is a reliable and dynamic marker of response that can be useful to optimize azacytidine therapy. Azacitidine 104-115 phospholipase C beta 1 Homo sapiens 3-11 22033492-1 2012 Phosphoinositide-phospholipase C (PI-PLC) beta1 can be considered a specific target for demethylating therapy in high-risk myelodysplastic syndrome (MDS) patients, as azacitidine treatment has been associated with a PI-PLCbeta1-specific promoter demethylation, and induction of PI-PLCbeta1 gene and protein expression. Azacitidine 167-178 phospholipase C beta 1 Homo sapiens 219-227 22033492-1 2012 Phosphoinositide-phospholipase C (PI-PLC) beta1 can be considered a specific target for demethylating therapy in high-risk myelodysplastic syndrome (MDS) patients, as azacitidine treatment has been associated with a PI-PLCbeta1-specific promoter demethylation, and induction of PI-PLCbeta1 gene and protein expression. Azacitidine 167-178 phospholipase C beta 1 Homo sapiens 281-289 22033492-2 2012 However, little is known about the molecular effect of azacitidine in low-risk MDS or the functional mechanisms linked with azacitidine effect on PI-PLCbeta1 promoter. Azacitidine 124-135 phospholipase C beta 1 Homo sapiens 149-157 22033492-4 2012 We first examined the effect of azacitidine on PI-PLCbeta1 promoter methylation and gene expression in low-risk MDS. Azacitidine 32-43 phospholipase C beta 1 Homo sapiens 50-58 22033492-6 2012 By applying a chromatin immunoprecipitation method, we also studied the correlation between the demethylating effect of azacitidine and the degree of recruitment to PI-PLCbeta1 promoter of some transcription factors implicated in hematopoietic stem cell proliferation and differentiation, as well as of the methyl-CpG-binding domain proteins, which specifically interact with methylated DNA. Azacitidine 120-131 phospholipase C beta 1 Homo sapiens 168-176 22033492-7 2012 Taken together, our results hint at a specific involvement of PI-PLCbeta1 in epigenetic mechanisms, and are particularly consistent with the hypothesis of a role for PI-PLCbeta1 in azacitidine-induced myeloid differentiation. Azacitidine 181-192 phospholipase C beta 1 Homo sapiens 169-177 19805378-3 2009 Also, a single patient treated with azacitidine, a DNA methyltransferase inhibitor currently used in MDS, displayed a direct correlation between PI-PLCbeta1 gene expression and drug responsiveness. Azacitidine 36-47 phospholipase C beta 1 Homo sapiens 148-156 21109771-0 2011 Synergistic induction of PI-PLCbeta1 signaling by azacitidine and valproic acid in high-risk myelodysplastic syndromes. Azacitidine 50-61 phospholipase C beta 1 Homo sapiens 28-36 21109771-4 2011 Indeed, AZA as a single agent was able to induce PI-PLCbeta1 expression, therefore providing a promising new tool in the evaluation of response to demethylating therapies. Azacitidine 8-11 phospholipase C beta 1 Homo sapiens 52-60 21109771-5 2011 In this study, we assessed the efficacy of the combination of AZA and VPA on inducing PI-PLCbeta1 expression in high-risk MDS patients. Azacitidine 62-65 phospholipase C beta 1 Homo sapiens 89-97 21109771-6 2011 Furthermore, we observed an increase in Cyclin D3 expression, a downstream target of PI-PLCbeta1 signaling, therefore suggesting a potential combined activity of AZA and VPA in high-risk MDS in activating PI-PLCbeta1 signaling, thus affecting cell proliferation and differentiation. Azacitidine 162-165 phospholipase C beta 1 Homo sapiens 88-96 21109771-6 2011 Furthermore, we observed an increase in Cyclin D3 expression, a downstream target of PI-PLCbeta1 signaling, therefore suggesting a potential combined activity of AZA and VPA in high-risk MDS in activating PI-PLCbeta1 signaling, thus affecting cell proliferation and differentiation. Azacitidine 162-165 phospholipase C beta 1 Homo sapiens 208-216 19805378-7 2009 Also, the molecular response correlated to and anticipated the clinical outcome, thus suggesting that PI-PLCbeta1 gene reactivation could predict azacitidine responsiveness. Azacitidine 146-157 phospholipase C beta 1 Homo sapiens 105-113 19805378-8 2009 Our results demonstrate not only that PI-PLCbeta1 promoter is hypermethylated in high-risk MDS patients, but also that the amount of PI-PLCbeta1 mRNA could predict the clinical response to azacitidine, therefore indicating a promising new therapeutic approach. Azacitidine 189-200 phospholipase C beta 1 Homo sapiens 41-49 19805378-8 2009 Our results demonstrate not only that PI-PLCbeta1 promoter is hypermethylated in high-risk MDS patients, but also that the amount of PI-PLCbeta1 mRNA could predict the clinical response to azacitidine, therefore indicating a promising new therapeutic approach. Azacitidine 189-200 phospholipase C beta 1 Homo sapiens 136-144 17625605-0 2008 PI-PLCbeta-1 and activated Akt levels are linked to azacitidine responsiveness in high-risk myelodysplastic syndromes. Azacitidine 52-63 phospholipase C beta 1 Homo sapiens 3-12