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Article

PI-PLCβ-1 and activated Akt levels are linked to azacitidine responsiveness in high-risk myelodysplastic syndromes

12 Jul 2007

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Identifiers

PMID: 17625605
DOI: 10.1038/sj.leu.2404855

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PI-PLCβ-1 and activated Akt levels are linked to azacitidine responsiveness in high-risk myelodysplastic syndromesPMID 17625605Read ↗

Synergistic induction of PI-PLCβ1 signaling by azacitidine and valproic acid in high-risk myelodysplastic syndromesSemantic proximity Read ↗

Epigenetic regulation of nuclear PI-PLCbeta1 signaling pathway in low-risk MDS patients during azacitidine treatmentSemantic proximity Read ↗

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Prospective phase II Study on 5-days azacitidine for treatment of symptomatic and/or erythropoietin unresponsive patients with low/INT-1-risk myelodysplastic syndromes.Semantic proximity Read ↗

Integrative Genomics Identifies the Molecular Basis of Resistance to Azacitidine Therapy in Myelodysplastic SyndromesSemantic proximity Read ↗

Prognostic implications of mono-hit and multi-hit TP53 alterations in patients with acute myeloid leukemia and higher risk myelodysplastic syndromes treated with azacitidine-based therapySemantic proximity Read ↗

Role of BCL2L10 methylation and TET2 mutations in higher risk myelodysplastic syndromes treated with 5-AzacytidineSemantic proximity Read ↗

Response of high-risk MDS to azacitidine and lenalidomide is impacted by baseline and acquired mutations in a cluster of three inositide-specific genes.Semantic proximity Read ↗

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