Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-20987
PROVIDER: PRJNA232634 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A mechanistic rationale for targeting the unfolded protein response in pre-B acute lymphoblastic leukemia [HTS]
| PRJNA232635 | ENA
Project description:Germline Aberrations of PAX5 Cause Susceptibility to pre-B cell Acute Lymphoblastic Leukemia
2015-07-13 | E-GEOD-45834 | ExpressionAtlas
Project description:Glucocorticoids induced transcriptional regulation in acute lymphoblastic leukemia
2025-01-16 | E-MTAB-9250 | ExpressionAtlas
Project description:Transcription profiling by array of human acute lymphoblastic leukemia and normal haemopoietic samples using Agilent Whole Human Genome Oligo Microarrays
2025-01-23 | E-MTAB-4006 | ExpressionAtlas
Project description:Gene expression profile of acute lymphoblastic leukemia cell lines treated with panobinostat
2025-01-24 | E-GEOD-26790 | ExpressionAtlas
Project description:Targeting epigenetic networks mediated by Prmt1 and Kdm4c in acute myeloid leukemia
2019-05-14 | E-MTAB-3322 | ExpressionAtlas
Project description:Transcription profiling of human T-cell lymphoblastic leukemia, acute mylelogenous leukemia and Diffuse Large Cell Lymphoma cell lines after treatment with aplidin and/or cytarabine
2025-01-24 | E-GEOD-5681 | ExpressionAtlas
Project description:Acute lymphoblastic leukemia (ALL) is associated with significant morbidity and mortality necessitating further improvements in diagnosis and therapy. Targeted therapies directed against epigenetic regulators, which are frequently mutated or misregulated in acute leukemia, are emerging as candidate approaches in preclinical studies and early trials. However, the epigenetic factors involved in most ALLs are not well defined or functionally characterized. In this study, we demonstrate an oncogenic role for the protein lysine methyltransferase SETDB2 in leukemia pathogenesis. It is over-expressed in a wide spectrum of leukemias, required for their maintenance in vitro and in vivo, and its elevated expression correlates with a poor prognosis in clinical cohorts. In a subset of ALL with the preBCR+ phenotype, SETDB2 expression is maintained as a direct target gene of the chimeric transcription factor E2A-PBX1. In this subset, SETDB2 epigenetically suppresses expression of the cell cycle inhibitor CDKN2C through histone H3K9 tri-methylation thus establishing a novel oncogenic pathway subordinate to E2A-PBX1 that silences a major tumor suppressor in ALL. In contrast, SETDB2 was relatively dispensable for normal hematopoietic stem and progenitor cell proliferation. In addition to targeting SETDB2 alone, its knockdown significantly enhanced sensitivity to kinase and epigenetic inhibitors suggesting a potential approach to future combination treatments. Our studies define an epigenetic role for SETDB2 in leukemia pathogenesis, and provide a mechanistic rationale for targeting SETDB2 therapeutically in a subset of leukemia.
2018-05-30 | GSE102947 | GEO
Project description:Transcription profiling by array of human T lymphoblastic leukemia Molt4 cells treated with vehicle or farnesol
2025-01-24 | E-GEOD-46670 | ExpressionAtlas