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• W1999044661 abstract "Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, ILAltered expression of microRNAs (miRNAs, a class of small regulatory RNAs) is associated with various types of cancers, including acute myeloid leukemia (AML). In our previous bead-based miRNA expression profiling assay, we observed that miR-181a, b, c, and d were all expressed at a higher level in the favorable prognosis subtypes of cytogenetically abnormal AML (CA-AML) carrying t(8;21), inv(16), or t(15;17) than in an intermediate- to poor-risk subtype of CA-AML harboring MLL rearrangements. Indeed, we found that increased expression of miR-181a or miR-181b was significantly (P<0.05) associated with longer OS in univariable testing, whereas only that of miR-181b remained significant (P<0.05) upon multivariable testing, after adjusting for other clinical, cytogenetic, and molecular variables. Through correlating expression of miR-181b with those of miR-181 putative target genes in 35 CA-AML patient samples, we identified 159 genes that exhibited a significantly inverse (P<0.05; Pearson Correlation) correlation of expression with miR-181b. PBX3 has the most significant inverse correlation with the expression of miR-181b, so we chose PBX3 as an important candidate target of miR-181 for further studies. We conducted luciferase reporter and mutagenesis assays and showed that PBX3 is a direct target of miR-181a/b. We also showed that forced expression of miR-181a/b significantly down-regulated endogenous expression of PBX3 in MLL-rearranged leukemic cells at both the RNA and protein levels. Ectopic expression of miR-181b significantly (P<.05) promoted apoptosis and decreased viability of MONOMAC-6/t(9;11), THP-1/t(9;11), and KOCL-48/t(4;11), and delayed leukemogenesis in MLL-fusion-mediated mouse leukemia model; such effects could be reversed by forced expression of PBX3 coding region. Our data suggest that the silencing of miR-181b and thereby the activation of the target genes, such as PBX3, likely contributes to the poor prognosis of adverse CA-AML patients. Thus, restoring expression of miR-181b and/or targeting the PBX3 pathways in poor prognosis AML patients may provide new strategies to improve outcome substantially.Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2309. doi:1538-7445.AM2012-2309" @default.
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• W1999044661 date "2012-04-15" @default.
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• W1999044661 title "Abstract 2309: Down-regulation of miR-181b contributes to the poor prognosis of adverse cytogenetically abnormal acute myeloid leukemia by targetingPBX3" @default.
• W1999044661 doi "https://doi.org/10.1158/1538-7445.am2012-2309" @default.
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