Millie: Search Results

Contributors : Christina D Drenberg ; Tanja A Gruber Series Type : Expression profiling by high throughput sequencing Organism : Homo sapiens. AML cell lines that underwent high throughput drug screening had baseline RNA sequencing done for the purpose of gene expression studies.

Series Type : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencing Organism : Mus musculus. This SuperSeries is composed of the SubSeries listed below.

Contributors : Robert Burns ; Luke Christiansen ; Jesus Izaguirre-Carbonell Series Type : Genome binding/occupancy profiling by high throughput sequencing Organism : Mus musculus. We performed genome-wide profiling of H3K9me3, H3K9me1, H3K27me3, and H3K36me3 by ChIP-seq in JMJD1C knockout or mutated MLL-AF9 leukemia cells.

Contributors : Robert Burns ; Luke Christiansen ; Jesus Izaguirre-Carbonell Series Type : Expression profiling by high throughput sequencing Organism : Mus musculus. We transduced clonally MLL-AF9 leukemia cells expressing cas9 with sgRNA targeting the jumonji and zinc finger domains of JMJD1C.

Contributors : Kim R Kampen ; Laura Fancello ; Tiziana Girardi ; Fabricio Loayza ; Benno Verbelen ; Stijn Vereecke ; Gianmarco Rinaldi ; Jelle Verbeeck ; Joyce O de Beeck ; Karin Thevissen ; Bruno Cammue ; Pieter Vermeersch ; David Cassiman ; Jan Cools ; Sarah-Maria Fendt ; Reuven Agami ; Mark Fiers ; Kim De Keersmaecker Series Type : Expression profiling by high throughput sequencing Organism : Mus musculus. Somatic ribosomal protein defects have recently been described in cancer, yet their impact on cellular transcription and translation remain poorly understood.

Series Type : Expression profiling by high throughput sequencing ; Other Organism : Mus musculus. This SuperSeries is composed of the SubSeries listed below.

By contrast, expression of KMT2A-MLLT3 alone cause ALL, double-positive leukemia (DPL, expressing both CD33 and CD19), or bilineal leukemia (BLL, comprised of distinct myeloid and lymphoid leukemia cells), and rarely AML.

Contributors : Ramin Radpour ; Adrian F Ochsenbein Series Type : Expression profiling by array Organism : Homo sapiens. We performed a comprehensive transcriptomic profiling of BM derived leukemia stem cells (LSCs) and leukemia progenitor cells (LPCs) together with paired CD8+ T cells of AML patients from different molecular risk groups.

Contributors : Arko Sen ; Graham McVicker Series Type : Genome binding/occupancy profiling by high throughput sequencing Organism : Homo sapiens. We performed ATAC-seq on publicly available leukemia cell-lines and used them to predict non-coding regulatory mutations in open-chromatin regions of the genome.

Bone marrow cells from moribund mice were harvested and labeled with anti-CD123 and anti-CD33 antibodies followed by cell sorting with the ARIA sorter.

Contributors : Biniam Adane ; Craig T Jordan Series Type : Expression profiling by high throughput sequencing Organism : Mus musculus. To investigate the function of NOX2 (CYBB) in leukemia stem cells, we created leukemia by tranforming primitive hematopoetic cells isolated from wild type and NOX2-KO mice with NUP98/HOXA9 and BCR/ABL oncogenes, isolated mRNA, and performed RNA-seq experiments to profile transcriptional changes upon NOX2 loss.

Status Public on Mar 18, 2019 Title miR-7977 transfer alter the transcriptome in bone marrow mesenchymal stem cells.

Contributors : Corina Schneidawind ; Kathy-Ann Secker Series Type : Expression profiling by high throughput sequencing Organism : Homo sapiens. Previous studies have identified frequent MLL-AF4 chromosomal translocation breakpoints in patients. Using CRISPRscan, we designed different sgRNAs recognizing patient-specific sequences in intron 11 of the MLL and exon 3 of the AF4 genes, respectively. Using plasmid- and virus-free delivery of sgRNAs with Cas9 protein, we nucleofected CD34+ target cells derived from human umbilical cord blood. Following nucleofection, the cells were maintained in liquid culture supplemented with cytokines and chemokines optimized for growth of MLLr cells. On day 30 (MLL-AF4) of liquid culture, MLL translocations wer.

Contributors : Martina Konantz ; Claudia Lengerke Series Type : Expression profiling by array Organism : Homo sapiens. In vivo studies indicate that human acute myeloid leukaemia (AML) originates from subpopulations of neoplastic cells with stem cell properties, thereby laying the foundation for the cancer stem cell concept.

Status Public on Mar 13, 2019 Title Dependence on Myb expression is attenuated in myeloid leukemia with N-terminal CEBPA mutations Organism Mus musculus Experiment type Expression profiling by high throughput sequencing Summary Mutations altering the normal function of C/EBPα are frequent in acute myeloid leukaemia with normal karyotype.

In order to characterize the single cell heterogeneity in comparison to normal cord blood we preformed droplet based single cell RNA-seq of FACS sorted CD34+ cells using the 10x genomics platform.

Series Type : Expression profiling by high throughput sequencing Organism : Homo sapiens. This SuperSeries is composed of the SubSeries listed below.

Contributors : Adam Mead ; Benjamin Povinelli Series Type : Expression profiling by high throughput sequencing Organism : Homo sapiens. We report on the characterization of JMML hematopoietic stem and progenitor cells (HSPCs). In order to molecularly characterize these populations we preformed bulk RNA-seq on purified cord blood and JMML HSCs, GMPs, and JMML double positives (+/+). We identified a conserved molecular hierarchy in JMML with high stem cell gene expression in HSCs, high progenitor and cell cycle gene expression in GMPs. We identified enriched gene sets in JMML HSCs vs CB HSCs, and find a number of potential therapeutic targets expressed in JMML.

Contributor : Frank A Middleton Series Type : Non-coding RNA profiling by high throughput sequencing Organism : Homo sapiens. We collected peripheral blood samples from 10 adult patients with newly diagnosed acute myeloid leukemia (AML), prior to induction chemotherapy, and 9 controls.

Here we show that a transcriptional regulator overexpressed in human myeloid malignancies, PRDM16s, causes oncogenic fate conversion, by transforming cells fated to form platelets and erythrocytes into myeloid leukemia-initiating cells (LICs.

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