Project description:Patients with acute myeloid leukemia and low circulating white count have a different gene expression profile compared those with high white count
Project description:Gene Expression Classifiers for Minimal Residual Disease and Relapse Free Survival Improve Outcome Prediction and Risk Classification in Children with High Risk Acute Lymphoblastic Leukemia: A Children's Oncology Group Study willm-00140 Assay Type: Gene Expression Provider: Affymetrix Array Designs: HG-U133_Plus_2 Organism: Homo sapiens (ncbitax) Tissue Sites: Blood, Bone marrow Material Types: Peripheral Blood, Bone Marrow Disease States: Childhood Precursor B-Lymphoblastic Leukemia
Project description:ERG is an Ets-transcription factor required for normal blood stem cell development. High ERG expression in acute myeloid leukemia (AML) and acute T-cell lymphoblastic leukemia (T-ALL) is associated with a stem cell signature and poor prognosis. In murine over-expression models, human ERG is a potent oncogene that induces both T-ALL and AML. However the functional and molecular consequences of high ERG expression in normal hematopoietic stem/progenitors (HSPCs), and how this contributes to leukemia development, are unknown. Here we show that retroviral transduction of ERG into human CD34+ cells and maintenance of ERG at levels present in high ERG AML results in altered myeloid and T cell differentiation and an increase in the self-renewal capacity of transduced progenitors but not the more primitive stem cell compartment. Integrated analysis of genome-wide expression in high ERG CD34+ and ERG binding profiles in HSPCs revealed that these functional characteristics were accompanied by an expression signature that was enriched in normal HSCs, high ERG AMLs, early T-cell precursor (ETP)-ALLs and leukemic stem cell signatures associated with poor clinical outcome. The proliferative advantage of high ERG progenitors may provide a cellular context for the acquisition and propagation of mutations that contribute to the pathogenesis of leukaemia. RNA sequencing in ERG overexpressing human CD34+ cells
Project description:Early T-cell precursor acute lymphoblastic leukemia (ETP-ALL) is a high-risk T-ALL subtype with distinct immunophenotypes and genetic alterations, complicating diagnosis and treatment. Although cytogenetic and gene expression studies have advanced the diagnostic and therapeutic strategies, the proteomics signatures of ETP-ALL remain underexplored. Herein, we performed 4D label-free proteomic analyses on mononuclear cells isolated from ETP-ALL, T-ALL, acute myeloid leukemia (AML), and healthy donor samples to identify molecular signatures specific to ETP-ALL.
Project description:Proteogenomic analysis and genomic profiling, RNA-sequencing, and mass spectrometry-based analysis of High hyperdiploid childhood acute lymphoblastic leukemia.
Project description:Gene expression profiling (GEP) can reveal characteristic signatures associated with distinct biologic subtypes of acute lymphoblastic leukemia (ALL). We performed GEP on Down syndrome (DS) and comparison non-Down syndrome (NDS) ALL cases to identify biologic differences between these groups. Ficoll-enriched, cryopreserved diagnostic bone marrow samples were obtained from patients with newly diagnosed B-precursor acute lymphoblastic leukemia.
Project description:Genome binding/occupancy profiling of ETS Variant Transcription Factor 6- Runt Related Transcription Factor 1 fusion protein (ETV6-RUNX1) in REH cells by high throughput sequencing. ETV6-RUNX1 is expressed in pediatric t(12;21) ETV6-RUNX1 B cell precursor acute lymphoblastic leukemia.
Project description:We determined the genome-wide digital gene expression (DGE) profiles of primary acute lymphoblastic leukemia (ALL) cells from 28 patients and fractionated blood cells from healthy blood donors taking advantage of “second generation” sequencing technology. The patients included in the study represent distinct subtypes of B-cell precursor (BCP) ALL and T-cell lineage ALL (T-ALL) and the controls are fractionated CD19+ and CD3+ cells.
