Michael D. Radmacher

TL;DR: A microRNA signature in molecularly defined, high-risk, cytogenetically normal AML is associated with the clinical outcome and with target genes encoding proteins involved in specific innate-immunity pathways.

TL;DR: Overall, this study showed that low pH accelerates acid consumption and proton export, while coinducing oxidative stress and heat shock regulons; (ii) high pH Accelerates proton import, while repressing the energy-expensive flagellar and chemotaxis regulons%; and (iii) pH differentially regulates a large number of periplasmic and envelope proteins.

TL;DR: A novel gene-expression signature is presented that offers additional prognostic information for patients with CN-AML and retained its significance in a multivariate model for OS.

TL;DR: The gene- and microRNA-expression profiles suggest that NPM1 mutations constitute a marker defining a biologically homogeneous entity in CN-AML that might be treated with specific and/or targeted therapies across age groups.

TL;DR: TET2 mutations improve the ELN molecular-risk classification in primary CN-AML because of their adverse prognostic impact in an otherwise favorable-risk patient subset and suggest that these patients may be candidates for alternative therapies.