Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-37363
PROVIDER: PRJNA159731 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:TET2 loss-of-function mutations associate with a DNA hypermethylation signature in diffuse large B-cell lymphoma (mRNA)
| PRJNA159821 | ENA
Project description:TET2 loss-of-function mutations associate with a DNA hypermethylation signature in diffuse large B-cell lymphoma (DNA methylation)
| PRJNA159819 | ENA
Project description:Transcription profiling by array of TET2 wild type and TET2 mutant patients with diffuse large B-cell derived lymphoma
2025-01-24 | E-GEOD-37363 | ExpressionAtlas
Project description:Cancer-associated IDH mutations are characterized by neomorphic enzyme activity and resultant 2 hydroxyglutarate (2HG) production. Mutational and epigenetic profiling of a large AML patient cohort revealed that IDH1/2-mutant AMLs display global DNA hypermethylation and a specific hypermethylation signature. Furthermore, expression of 2HG-producing IDH alleles in cells rapidly induced global DNA hypermethylation. In the AML cohort, IDH1/2 mutations were mutually exclusive with mutations in the α-ketoglutarate-dependent enzyme TET2, and TET2 loss-of function mutations associated with similar epigenetic defects as IDH1/2 mutants. Consistent with these genetic and epigenetic data, expression of IDH mutants impaired TET2 catalytic function in cells. Finally, either expression of mutant IDH1/2 or Tet2 depletion impaired hematopoietic differentiation and increased stem cell marker expression, suggesting a shared pro-leukemogenic effect. DNA methylation and gene expression profiling in IDH1/2 mutant vs. IDH1/2 wild-type AML
2010-12-03 | E-GEOD-24505 | biostudies-arrayexpress
Project description:Cancer-associated IDH mutations are characterized by neomorphic enzyme activity and resultant 2 hydroxyglutarate (2HG) production. Mutational and epigenetic profiling of a large AML patient cohort revealed that IDH1/2-mutant AMLs display global DNA hypermethylation and a specific hypermethylation signature. Furthermore, expression of 2HG-producing IDH alleles in cells rapidly induced global DNA hypermethylation. In the AML cohort, IDH1/2 mutations were mutually exclusive with mutations in the α-ketoglutarate-dependent enzyme TET2, and TET2 loss-of function mutations associated with similar epigenetic defects as IDH1/2 mutants. Consistent with these genetic and epigenetic data, expression of IDH mutants impaired TET2 catalytic function in cells. Finally, either expression of mutant IDH1/2 or Tet2 depletion impaired hematopoietic differentiation and increased stem cell marker expression, suggesting a shared pro-leukemogenic effect.
2010-12-03 | GSE24505 | GEO
Project description:Knock-down of BCL6 expression in human Diffuse Large B-Cell Lymphoma cell lines
2025-01-24 | E-GEOD-45838 | ExpressionAtlas
Project description:Loss-of-function TET2 mutations (TET2MT) are common in myeloid neoplasia. TET2, a DNA dioxygenase, requires 2-oxoglutarate and Fe(II) to oxidize 5-methylcytosine. TET2MT thus result in hypermethylation and transcriptional repression. Ascorbic acid (AA) increases dioxygenase activity by facilitating Fe(III)/Fe(II) redox reaction and may alleviate some biological consequences of TET2MT by restoring dioxygenase activity. Here, we report the utility of AA in the prevention of TET2MT MN, clarify the mechanistic underpinning of the TET2-AA interactions, and demonstrate that the ability of AA to restore TET2 activity in cells depends on N- and C-terminal lysine acetylation and nature of TET2MT. Consequently, pharmacologic modulation of acetyltransferases and histone deacetylases may regulate TET dioxygenase-dependent AA effects. Thus, our study highlights the contribution of factors that may enhance or attenuate AA effects on TET2 and provides a rationale for novel therapeutic approaches including combinations of AA with class I/II HDAC inhibitor or sirtuin activators in TET2MT leukemia.
2020-09-09 | PXD020550 | Pride
Project description:Concomitant multiple hematological malignancies are rare and challenging to diagnose. They represent a unique model to explore the multistep process of oncogenesis. Here, we report the unique case of 62 years-old man with cardiac tamponade as first manifestation of ALK negative anaplastic large T-cell lymphoma (ALK- ALCL). Following chemotherapy, he showed one year later ALK- ALCL concurrent with diffuse large B-cell lymphoma (DLBCL-NOS) and acute monoblastic leukemia (AML-M5) in a single excisional lymph node. Clinical, pathological and multiomics data (whole exome and targeted deep sequencing, spatial transcriptomics) were analyzed. Two somatic TET2 gene mutations at high allele burden were shared by all three neoplasms, uninvolved bone marrow and CD34+ hematopoietic stem and progenitor cells (HSPCs). Secondary hits characterized each malignancy. ALK- ALCL (pericardial and nodal) showed TP53 and LYN deleterious mutations, DLBCL-NOS disclosed KRAS, STAT6, CREBBP and ATM alterations and AML-M5 had JAK3, PPM1D, NF1 and KMT2D mutations and a complex karyotype. Furthermore we demonstrated that spatial transcriptomics can identify the specific signatures of the three neoplasms. Two TET2 mutations at high allele burden in CD34+HSPCs conferred the favorable soil and the genotoxic stress from chemotherapy likely contributed to multiple hematological malignancies oncogenesis. Our case confirms the pathogenetic link between clonal hematopoiesis and cytotoxic T-cell lymphoma, so far only suspected. Most importantly, this is the first study to document the oncogenic phylogeny of concurrent T-, B-, and myeloid neoplasms from CD34+ HSPCs clone(s) in a single specimen.
2023-03-17 | E-MTAB-12742 | biostudies-arrayexpress
Project description:The distinction between the Burkitt lymphoma and diffuse large B-cell lymphoma is imprecise using current diagnostic criteria. We applied transcriptional and genomic profiling to molecularly define Burkitt lymphoma. Gene expression profiling employing Affymetrix GeneChips (U133A) was performed in 220 mature aggressive B-cell lymphomas, including a core group of eight Burkitt lymphomas, which fulfilled all diagnostic criteria of the WHO classification. A molecular signature of Burkitt lymphoma was generated. Chromosomal abnormalities were detected by interphase fluorescence in-situ hybridization and array comparative genomic hybridization. The molecular Burkitt lymphoma signature identified 44 cases. Fifteen of these cases lacked a morphology typical for Burkitt/Burkitt-like lymphoma. The vast majority (88%) of the 176 lymphomas without the molecular Burkitt lymphoma signature represented diffuse large B-cell lymphomas. In 20% of these cases a MYC break was detectable which was associated with complex chromosomal changes. Our molecular definition of Burkitt lymphoma sharpens and extends the spectrum of Burkitt lymphoma. In mature aggressive B-cell lymphomas without a Burkitt lymphoma signature, a chromosomal break in the MYC locus proved to be associated with adverse clinical outcome. Experiment Overall Design: 220 diffuse large B-cell lymphoma and Burkitt lymphoma samples hybridized to 221 HGU133A Affymetrix GeneChips
2008-06-13 | E-GEOD-4475 | biostudies-arrayexpress
Project description:A multi-omics approach to decipher the complexity of drug resistance in diffuse large B-cell lymphoma
2025-01-23 | E-MTAB-6597 | ExpressionAtlas