about
The lncRNA CASC15 regulates SOX4 expression in RUNX1-rearranged acute leukemia.BAG1: the guardian of anti-apoptotic proteins in acute myeloid leukemia.LncRNA Expression Discriminates Karyotype and Predicts Survival in B-Lymphoblastic Leukemia.RNA-binding protein IGF2BP3 targeting of oncogenic transcripts promotes hematopoietic progenitor proliferation.MicroRNA-34b promoter hypermethylation induces CREB overexpression and contributes to myeloid transformation.Hh/Gli antagonist in acute myeloid leukemia with CBFA2T3-GLIS2 fusion gene.Pediatric non-Down syndrome acute megakaryoblastic leukemia is characterized by distinct genomic subsets with varying outcomes.MLL-AF6 fusion oncogene sequesters AF6 into the nucleus to trigger RAS activation in myeloid leukemia.DHH-RHEBL1 fusion transcript: a novel recurrent feature in the new landscape of pediatric CBFA2T3-GLIS2-positive acute myeloid leukemia.Prognostic significance of flow-cytometry evaluation of minimal residual disease in children with acute myeloid leukaemia treated according to the AIEOP-AML 2002/01 study protocol.ZNF521 sustains the differentiation block in MLL-rearranged acute myeloid leukemia.Genomic complexity and dynamics of clonal evolution in childhood acute myeloid leukemia studied with whole-exome sequencing.Identification of the NUP98-PHF23 fusion gene in pediatric cytogenetically normal acute myeloid leukemia by whole-transcriptome sequencing.Infants with acute myeloid leukemia treated according to the Associazione Italiana di Ematologia e Oncologia Pediatrica 2002/01 protocol have an outcome comparable to that of older children.DNA methyltransferase 3a hot-spot locus is not mutated in pediatric patients affected by acute myeloid or T-cell acute lymphoblastic leukemia: an Italian study.Minimal residual disease monitored after induction therapy by RQ-PCR can contribute to tailor treatment of patients with t(8;21) RUNX1-RUNX1T1 rearrangement.CBFA2T3-GLIS2 fusion transcript is a novel common feature in pediatric, cytogenetically normal AML, not restricted to FAB M7 subtype.Results of the AIEOP AML 2002/01 multicenter prospective trial for the treatment of children with acute myeloid leukemia.Screening of novel genetic aberrations in pediatric acute myeloid leukemia: a report from the AIEOP AML-2002 study group.Characterization of children with FLT3-ITD acute myeloid leukemia: a report from the AIEOP AML-2002 study group.Targeting BAG-1: a novel strategy to increase drug efficacy in acute myeloid leukemia.CREB engages C/EBPδ to initiate leukemogenesis.Epigenetic heterogeneity affects the risk of relapse in children with t(8;21)RUNX1-RUNX1T1-rearranged AML.ICER evokes Dusp1-p38 pathway enhancing chemotherapy sensitivity in myeloid leukemia.Core-binding factor acute myeloid leukemia in pediatric patients enrolled in the AIEOP AML 2002/01 trial: screening and prognostic impact of c-KIT mutations.NUP98-fusion transcripts characterize different biological entities within acute myeloid leukemia: a report from the AIEOP-AML groupWhole transcriptome sequencing of a paediatric case of de novo acute myeloid leukaemia with del(5q) reveals RUNX1-USP42 and PRDM16-SKI fusion transcriptsA Case of T-cell Acute Lymphoblastic Leukemia Relapsed As Myeloid Acute LeukemiaMLL partner genes drive distinct gene expression profiles and genomic alterations in pediatric acute myeloid leukemia: an AIEOP studyDrp1 Controls Effective T Cell Immune-Surveillance by Regulating T Cell Migration, Proliferation, and cMyc-Dependent Metabolic ReprogrammingcAMP response element binding protein (CREB) overexpression CREB has been described as critical for leukemia progressionICER expression inhibits leukemia phenotype and controls tumor progressionPresence of high-ERG expression is an independent unfavorable prognostic marker in MLL-rearranged childhood myeloid leukemiaTwo consecutive immunophenotypic switches in a child with MLL-rearranged acute lymphoblastic leukemiaPrognostic impact of t(16;21)(p11;q22) and t(16;21)(q24;q22) in pediatric AML: a retrospective study by the I-BFM Study Group
P50
Q33919296-C02CF34F-4406-4561-8B23-E8B7672C2A56Q34053504-9E16E54C-259D-4936-8129-96CB768A6182Q35611421-3236EDC2-01E9-40CE-A445-EC41BF1936CFQ36737959-5CCDA859-6425-40E3-BF0E-3BFAE19F636CQ36862518-1DE819B0-3671-41AE-BB0B-B0BAA6C8D5CAQ37597243-CE0433D1-C375-4665-BB1C-0EBFDF35431BQ39005643-25359787-A1CF-4DEE-ACCE-5BC2860C17ECQ39008746-90AB1D49-778F-40D1-A281-480C56316448Q39221970-CA1A911A-0FAF-4FED-8664-92250C32AD4FQ40316983-EE2B1ACA-1686-4283-963A-0D88F80834F4Q42265722-E5CDE3C4-37EA-4D89-B2A0-34C5E539B3D7Q42322251-9F96D3D0-952E-4499-8886-4BDFDAF89819Q42434309-02B95416-6F78-4DEF-9903-81D69BD4D5C3Q42759144-AC26D65D-C304-4743-8E9A-5E595FA4B62FQ43004456-0796BC2D-23EA-4BA8-A201-80D7B4A29896Q43175202-41810977-620F-4417-A2B4-A31F62D60C0BQ44198608-013FC2D9-3672-4B35-9E60-1548F3532A43Q44563856-8BFC00E5-50C4-46A0-8729-570D5A5D9164Q47817382-656B90B2-A764-46C1-ADC8-4009324ABABEQ48159392-F64DD18C-2783-4F78-B120-809E8C0C40BFQ51029263-60E1184E-8ECE-4ADC-A138-5ED71C103B9AQ52671045-B37EE7E3-5684-460C-9BA0-2D705A79D312Q52689080-59D5DC06-63E3-4680-A78D-A356BDD375ACQ53267724-3F24FA81-1211-4208-892F-7532A832F478Q54397201-F2D3A0E2-3F7F-4D52-979D-486947D75EDEQ56960711-3F1CD13B-DFCE-4E39-88ED-93817B4217CEQ56973354-0E620655-567C-4761-B4DB-8096DAAE75FFQ60146455-97B78394-0035-4D29-B18C-61A0D2DE46EBQ60170373-A6546661-4025-493A-A405-49BBE3DA996FQ60303325-030DF4F6-74AD-4091-8833-9776D327EEE1Q79909092-B6AF6617-71F9-42C2-AF8D-E0F15F090136Q81951836-0AB75776-47B6-4DBF-B7E6-E79BFAA457AEQ83336491-98E7AD4D-168D-4113-89D2-9E8ADCE123D5Q83366957-FA4749B1-0511-49E1-82BF-1C548D6181A1Q91164151-605F0FF1-1F42-4AE0-9567-E4DE6F625978
P50
description
hulumtuese
@sq
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Martina Pigazzi
@ast
Martina Pigazzi
@en
Martina Pigazzi
@es
Martina Pigazzi
@nl
type
label
Martina Pigazzi
@ast
Martina Pigazzi
@en
Martina Pigazzi
@es
Martina Pigazzi
@nl
prefLabel
Martina Pigazzi
@ast
Martina Pigazzi
@en
Martina Pigazzi
@es
Martina Pigazzi
@nl
P106
P21
P31
P496
0000-0002-4793-5263