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A rare location, t(6;11)(q27;q23) (MLL-AF6), is associated with poor outcome in childhood acute myeloid leukemia (AML). The described mechanism by which MLL-AF6, through constitutive self-association and in cooperation with DOT-1L, activates aberrant gene expression does not explain the biological differences existing between t(6;11)-rearranged and other(More)
cAMP response element binding protein (CREB) is frequently overexpressed in acute myeloid leukemia (AML) and acts as a proto-oncogene; however, it is still debated whether such overactivation alone is able to induce leukemia as its pathogenetic downstream signaling is still unclear. We generated a zebrafish model overexpressing CREB in the myeloid lineage,(More)
Modena, Modena, Italy), Dr Aroldo Rizzo (Pathology Unit, Ospedale Cervello, Palermo, Italy), Dr Maria Teresa Enrica Martini (Pathology Unit, Ospedale Santo Spirito Regina Margherita, Rome, Italy), Dr Anna Guidetti (Oncologia Medica 3, Istituto Nazionale dei Tumori, Milan, Italy), Dr Andrea Carnevali (Pathology Unit, Azienda Ospedaliera di Arezzo, Arezzo,(More)
The genomic landscape of children with acute myeloid leukemia (AML) who do not carry any cytogenetic abnormality (CN-AML) is particularly heterogeneous and challenging, being characterized by different clinical outcomes. To provide new genetic insights into this AML subset, we analyzed through RNA-seq 13 pediatric CN-AML cases, corroborating our findings in(More)
Taurine from natural sources has gained great importance as essential nutrient in milk for formula-fed infants. There is a strong request for a method capable of determining the natural origin of taurine. The measure of beta-radioactivity of 14C of taurine by means of liquid scintillation counting proved the most reliable. A simple method is reported.
Recurrent molecular markers have been routinely used in acute myeloid leukemia (AML) for risk assessment at diagnosis, whereas their post-induction monitoring still represents a debated issue. We evaluated the prognostic value and biological impact of minimal residual disease (MRD) and of the allelic ratio (AR) of FLT3-internal-tandem duplication (ITD) in(More)
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