Gruber AML WGS - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001006442 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:RNASeq files for paper titled "Integrative Analysis of Pediatric Acute Leukemia Identifies Acute Myeloid/T-Lymphoblastic Leukemia Subtype that Spans a T Lineage and Myeloid Continuum with Distinct Prognoses"
| EGAD00001006444 | EGA
Project description:WXS files for paper titled "Integrative Analysis of Pediatric Acute Leukemia Identifies Acute Myeloid/T-Lymphoblastic Leukemia Subtype that Spans a T Lineage and Myeloid Continuum with Distinct Prognoses"
| EGAD00001006443 | EGA
Project description:This SuperSeries is composed of the following subset Series: GSE30745: Expression data from murine acute myeloid leukemia (AML) cells following shRNA-mediated suppression of Myb GSE30746: Expression data from murine Tet-off MLL-AF9/Ras acute myeloid leukemia cell lines following withdrawal of MLL-AF9 Refer to individual Series
2011-08-04 | E-GEOD-30747 | biostudies-arrayexpress
Project description:Acute myeloid leukemia (AML) is the most common and severe acute leukemia in adults. It is a heterogeneous disease where the subset of molecularly different types, presenting various morphological features and differentiation stage, can be distinguished. Genomic research of leukemias is conducted since 1999 and large cohort studies shown that particular genetic alterations correspond with specific gene expression signatures. However, not always they provide clinically relevant information. The most unknown group is cytogenetically normal acute myeloid leukemia (CN-AML, 40-49% of all AML cases). The aim of our experiment was to determine selected gene expression profiles in CN-AML, using small, boutique microarray. The array contained 933 oligonucleotide probes, mainly complementary to acute myeloid leukemia markers, genes involved in leukemic transformation and myeloid cell proliferation, differentiation and maturation. Our test dataset included 40 hybridizations: 24 corresponding with blood and bone marrow samples collected from 12 patients with AML M1 or M2 FAB subtype and 16 corresponding with healthy control samples. Total RNA was extracted from the mononuclear cell fractions, reversibly transcribed to cDNA and labeled with Alexa 647 dye. The common reference was RNA isolated from HL-60 cell culture, labeled with Alexa 555 dye.
2013-07-01 | E-MEXP-3647 | biostudies-arrayexpress
Project description:Microarrays transcriptomic data analyses from acute myeloid leukemia cell line OCI-AML2 and primary acute myeloid leukemia cells treated with actinomycin D.
2021-05-10 | E-MTAB-10397 | biostudies-arrayexpress
Project description:Acute myeloid leukemia (AML) is a heterogeneous disease in respect of molecular aberrations and prognosis. We used gene expression profiling of 562 patients treated in the German AMLCG 1999 trial to develop a gene signature that predicts survival in AML. Analysis of 562 samples (140 HGU-133plus2; 422 HGU-133A; 422 HGU-133B) from adult patients with acute myeloid leukemia (AML).
2013-02-07 | E-GEOD-37642 | biostudies-arrayexpress
Project description:Background: The oncogenic protein HOXA9 plays a critical role in leukemia transformation and maintenance, and its aberrant expression is a hallmark of most aggressive acute leukemia. Although inhibiting the upstream regulators of HOXA9 has been proven as a significant therapeutic intervention, the comprehensive regulation network controlling HOXA9 expression in leukemia has not been systematically investigated. Results: Here, we perform genome-wide CRISPR/Cas9 screening in the HOXA9-driven reporter acute leukemia cells. We identify a poorly characterized RNA-binding protein, RBM5, as the top candidate gene required to maintain leukemia cell fitness. RBM5 is highly overexpressed in acute myeloid leukemia (AML) patients compared to healthy individuals. RBM5 loss triggered by CRISPR knockout and shRNA knockdown significantly impairs leukemia maintenance in vitro and in vivo. Through domain CRISPR screening, we reveal that RBM5 functions through a noncanonical transcriptional regulation circuitry rather than RNA splicing, such an effect depending on DNA-binding domains. By integrative analysis and functional assays, we identify HOXA9 as the downstream target of RBM5. Ectopic expression of HOXA9 rescues impaired leukemia cell proliferation upon RBM5 loss. Importantly, acute protein degradation of RBM5 through auxin-inducible degron system immediately reduces HOXA9 transcription. Conclusions: We identify RBM5 as a new upstream regulator of HOXA9 and reveal its essential role in controlling the survival of AML. These functional and molecular mechanisms further support RBM5 as a promising therapeutic target for myeloid leukemia treatment. Keywords: Acute myeloid leukemia; CRISPR screen; Genome editing; HOXA9; RBM5.
2023-11-16 | GSE225633 | GEO
Project description:Acute Myeloid Leukemia (AML) patient xenografts
| PRJNA736604 | ENA
Project description:The paper describes a model of acute myeloid leukaemia.
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This model is described in the article:
Optimal control of acute myeloid leukaemia
Jesse A. Sharp, Alexander P Browning, Tarunendu Mapder, Kevin Burrage, Matthew J Simpson
Journal of Theoretical Biology 470 (2019) 30–42
Abstract:
Acute myeloid leukaemia (AML) is a blood cancer affecting haematopoietic stem cells. AML is routinely treated with chemotherapy, and so it is of great interest to develop optimal chemotherapy treatment strategies. In this work, we incorporate an immune response into a stem cell model of AML, since we find that previous models lacking an immune response are inappropriate for deriving optimal control strategies. Using optimal control theory, we produce continuous controls and bang-bang controls, corre- sponding to a range of objectives and parameter choices. Through example calculations, we provide a practical approach to applying optimal control using Pontryagin’s Maximum Principle. In particular, we describe and explore factors that have a profound influence on numerical convergence. We find that the convergence behaviour is sensitive to the method of control updating, the nature of the control, and to the relative weighting of terms in the objective function. All codes we use to implement optimal control are made available.
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2024-09-02 | BIOMD0000000798 | BioModels
Project description:Mixed phenotype acute leukemia (MPAL) also known as acute leukemia of ambiguous lineage (ALAL), is characterized by leukemic blasts with both lymphoid and myeloid cell surface markers. Here, we use SC multiomic profiling on newly diagnosed MPAL samples to characterize the immunophenotypic, genetic, and transcriptional landscapes of MPAL. This profiling allows us to definitively contradict the paradigm of MPAL as a disease on a continuum with myeloid and lymphoid lineage acute leukemias, and instead identifies MPAL as a distinct, stem-like disease that, unlike other leukemias, cannot be defined by genetics alone. We further describe a stem cell gene expression signature for MPAL that can predict patient survival. These results broaden our understanding of MPAL biology and suggest a path toward novel risk stratification for MPAL. Importantly, these findings have potential to direct treatment and, hopefully, ultimately improve the prognosis of this disease.
2024-03-13 | GSE261228 | GEO