Project description:Using RNA deep sequencing we determined gene expression patterns and expression genotypes in Acute Myeloid Leukemia (AML) cell lines harboring a 3q-aberration. These cell lines specifically overexpress the gene EVI1 which plays a significant part in leukomogenesis. Additionally we RNA sequenced AML cell lines that overexpress EVI1 resulting from different genetic causes or do not express EVI1 at all.
Project description:MOLM-13 acute myeloid leukemia cells were treated with 3 µM FIDAS-5 methionine S-adenosyltransferase 2A (MAT2A) inhibitor or 0.1% DMSO as control for 48 hours
Project description:Label-free quantitation dataset from 44 representative Acute Myeloid Leukemia (AML) patients from the LAML TCGA dataset, and 6 healthy bone marrow derived controls including 3 lineage-depleted and 3 CD34+ selected bone marrows.
Project description:Azacytidine (AzaC) and decitabine (AzadC) are cytosine analogs that covalently trap DNA methyltransferases, which place the important epigenetic mark 5-methyl-2’-deoxycytidine by methylating 2’-deoxycytidine (dC) at the C5 position. AzaC and AzadC are used in the clinic as antimetabolites to treat myelodysplastic syndrome and acute myeloid leukemia and are explored against other types of cancer. Although their principal mechanism of action is known, the downstream effects of AzaC and AzadC treatment are not well understood and the cellular prerequisites that determine sensitivity towards AzaC and AzadC remain elusive. Here, we investigated the effects and phenotype of AzaC and AzadC exposure on the acute myeloid leukemia cell line MOLM-13. We found that while AzaC and AzadC share many effects on the cellular level, including decreased global DNA methylation, increased formation of DNA double strand breaks, transcriptional downregulation of important oncogenes and similar changes on the proteome level, AzaC failed in contrast to AzadC to induce apoptosis in MOLM-13. The only cellular marker that correlated with this clear phenotypical outcome was the level of hydroxy-methyl-dC, an additional epigenetic mark that is placed by TET enzymes and repressed in cancer cells. Whereas AzadC increased hmdC substantially in MOLM-13, AzaC treatment did not result in any increase at all. This suggests that hmdC levels in cancer cells should be monitored as a response towards AzaC and AzadC and considered as a biomarker to judge whether AzaC or AzadC lead to cell death in leukemic cells.
Project description:A deep-scale proteome and phosphoproteome database from 44 representative Acute Myeloid Leukemia (AML) patients from the LAML TCGA dataset, and 6 healthy bone marrow derived controls including 3 lineage-depleted and 3 CD34+ selected bone marrows.
Project description:The goal of this study was to determine the effects of gene deletions and duplications on acute myeloid leukemia cells immunogenicity. The Clones were derived from the C1498 AML cell line. Lymphocytes were isolated from the C57BL/6 mouse strain. Genome profiling of mouse single cell clones originating from an acute myeloid leukemia cell line compared to control T lymphocytes from the same murine strain.
Project description:The goal of this study was to determine the effects of gene deletions and duplications on acute myeloid leukemia cells immunogenicity. The Clones were derived from the C1498 AML cell line. Lymphocytes were isolated from the C57BL/6 mouse strain. Genome profiling of mouse single cell clones originating from an acute myeloid leukemia cell line compared to control T lymphocytes from the same murine strain.
Project description:Single-cell RNA sequencing was performed on bone marrow mononuclear of a patient with acute myeloid leukemia with erythroid differentiation of the blasts and on peripheral blood mononuclear cells of a patient with acute myeloid leukemia with megakaryocytic differentiation of the blasts. Raw data for this dataset can be found at the EGA under accession EGAS00001006819.