Project description:In an attempt to clarify the diferrence of exosomal microRNA derived from Normal BM and primary AML CD34+ cells. Primary cells were cultured in serum free medium and supernatant was harvested. After extract microRNAs, the difference of exosomal microRNAs between normal BM and leukemia was analyzed by array.
Project description:Acute myeloid leukemia (AML) cells release abundant exosomal miR-7977 that transfer into bone marrow (BM) mesenchymal stromal cells (MSCs). We have shown that exosomal miR-7977 was highly released from AML cells and was transferred into BM MSCs. It has been well known that a microRNA has multiple targets. In fact, miRDB predicted 633 targets. Based on these findings, control and miR-7977mimic were transferred into BM MSCs. Subsequently, alteration of transcriptome was analyzed to gain insight into the role of miR-7977 in bone marrow micro environment.
Project description:An Affymetrix microRNA (miRNA) Array was used to compare exosomal miRNAs released by hypothalamic stem/progenitor cells (htNSC), hippocampal NSC (hippoNSC) and astrocytes in primary culture. This assay is to provide preliminary information on the general profile of exosomal miRNAs released by these cells, while to study any particular miRNA species should require further quantitative analyses such as qPCR based on enough sample sizes.
Project description:Chip-chip data from primary human AML patient blasts, normal CD34+ HSCs, normal neutrophils and normal T cells with H3K9 and H3K27 antibodies. Gene expression profiling from primary human AML patient blasts and CD34+ normal cells. Analysis of the chromatin landscape of the ERG locus using H3K9 and H3K27 as markers of euchromatin and heterochromatin respectively. Analysis of ERG expression in AML patients with normal CD34+ HSCs as control.
Project description:Chip-chip data from primary human AML patient blasts, normal CD34+ HSCs, normal neutrophils and normal T cells with H3K9 and H3K27 antibodies. Gene expression profiling from primary human AML patient blasts and CD34+ normal cells. Analysis of the chromatin landscape of the ERG locus using H3K9 and H3K27 as markers of euchromatin and heterochromatin respectively. Analysis of ERG expression in AML patients with normal CD34+ HSCs as control. Correlation of the activity of a stem cell enhancer at the ERG locus in AML primary patient blasts with their transcriptome and clinical outcome data.
Project description:This paper presents a T-cell receptor (TCR) reactive to the recurrent D835Y driver mutation in the FLT3 tyrosine-kinase domain. TCRFLT3D/Y-redirected T cells selectively eliminated primary human AML cells harboring the D835Y mutation in vitro and in vivo. The TCRFLT3D/Y cells rejected both CD34+ and CD34- AML in mice engrafted with primary leukemia from patients, reaching minimal residual disease negative levels, and eliminated primary CD34+ AML leukemia-propagating cells in vivo. Thus, T cells targeting a single shared mutation can provide efficient immunotherapy towards selective elimination of clonally involved primary AML cells in vivo.
Project description:Acute myeloid leukemia (AML) is a heterogeneous group of diseases. Normal cytogenetics (CN) constitutes the single largest group, while trisomy 8 (+8) as a sole abnormality is the most frequent trisomy. How trisomy contributes to tumorigenesis is unknown. We used oligonucleotide-based DNA microarrays to study global gene expression in AML+8 patients with +8 as the sole chromosomal abnormality and AML-CN patients. CD34+ cells purified from normal bone marrow (BM) were also analyzed as a representative heterogeneous population of stem and progenitor cells. Expression patterns of AML patients were clearly distinct from those of CD34+ cells of normal individuals. We show that AML+8 blasts overexpress genes on chromosome 8, estimated at 32% on average, suggesting gene-dosage effects underlying AML+8. Systematic analysis by cellular function indicated up-regulation of genes involved in cell adhesion in both groups of AML compared with CD34+ blasts from normal individuals. Perhaps most interestingly, apoptosis-regulating genes were significantly down-regulated in AML+8 compared with AML-CN. We conclude that the clinical and cytogenetic heterogeneity of AML is due to fundamental biological differences. **NOTE: Migrated from caArray 1.x, identifier='gov.nih.nci.ncicb.caarray:Experiment:1015897559579654:1'
Project description:The label-free quantitative proteome was generated for 42 primary AML patient samples enriched for CD34+ cells (or mononuclear cells in the case of NPMcyt sameples) and as controls 6 mobilized peripheral blood CD34+ cells were included. Furthermore, 6 AML cell lines were included, and also primary mesenchymal stem cells grown under normaoxia or hypoxia were included.
Project description:Acute myeloid leukemia (AML) is a hematopoietic malignancy with a dismal outcome in the majority of cases. A detailed understanding of the genetic alterations and gene expression changes that contribute to its pathogenesis is important to improve prognostication, disease monitoring, and therapy. The expression of 636 human miRNAs was compared between samples from 52 patients with AML and 13 healthy individuals by locked nucleic acid (LNA) based microarray technology. 143 miRNAs were expressed at detectable levels, and 64 of these were significantly differentially expressed between AML and healthy peripheral blood, bone marrow, and/or CD34+ cells. Reference: A Rommer et al, Overexpression of primary microRNA 221/222 in acute myeloid leukemia, BMC Cancer, 2013. 52 AML, 5 peripheral blood (PB), 5 bone marrow (BM), and 3 CD34+ cell samples from healthy donors were subjected to miRNA microarray analysis.
Project description:The label-free quantitative proteome was generated for 30 primary AML patient samples enriched for CD34+ cells or CKIT+ cells in the case of NPMcyt samples. As controls 3 mobilized peripheral blood CD34+ cells were included.