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Methylation and gene expression data obtained from Dnmt3b+/- peripheral T-cell lymphomas.

ABSTRACT: Methylation and gene expression data obtained from Dnmt3b+/- peripheral T-cell lymphomas.

PROVIDER: PRJNA645699 | ENA |

REPOSITORIES: ENA

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Methylation and gene expression data obtained from Dnmt3b+/- peripheral T-cell lymphomas.

Project description:Dnmt3b is a tumor suppressor in oncogene-driven lymphoid and myeloid malignancies in mice. However, it is poorly understood whether reduced Dnmt3b activities can initiate malignant hematopoiesis. We modulated Dnmt3b activity in vivo by generating Dnmt3b+/− mice expressing one wild-type allele. Here, we analyzed methylation and gene expression in Dnmt3b+/- peripheral T-cell lymphomas (PTCLs).

2020-12-31 | GSE154270 | GEO

Methylation and gene expression data obtained from Dnmt3b+/+, Dnmt3bD/D and Dnmt3bCI/CI MYC induced T-cell lymphomas (MTCLs).

Project description:DNA methylation has suppressive effects on gene transcription and it is involved in a variety of physiologic processes, including development and cancer. As we and others demonstrated, Dnmt3b is a tumor suppressor in oncogene-driven lymphoid and myeloid malignancies in mice. Due to numerous activities such as methylation-dependent and independent repression and accessory functions, it is difficult to pinpoint physiological processes solely dependent on catalytic activity of Dnmt3b. By utilizing our new mouse model expressing catalytically inactive Dnmt3b at physiological levels we identified genome-wide methylation changes and aberrant gene expression profiles that are specific to catalytic activity of DNMT3b.

2020-12-30 | GSE154451 | GEO

Methylation and gene expression data obtained from Dnmt3b+/+, Dnmt3bD/D and Dnmt3bCI/CI MYC induced T-cell lymphomas (MTCLs).

Project description:Methylation and gene expression data obtained from Dnmt3b+/+, Dnmt3bD/D and Dnmt3bCI/CI MYC induced T-cell lymphomas (MTCLs).

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Methylation data from normal thymocytes, 24 day pre-tumor Dnmt3b-deficient thymocytes, Wild-Type Tumors, and Dnmt3b-deficient Tumors

Project description:Dnmt3b is a DNA methytransferase which is an enzyme that methylated genomic DNA which contributes to genomic stability and transcriptional regulation. We genetically inactivated Dnmt3b in the hematopoeitic compartment in the context of MYC overexpression and analysed the resulting thymic lymphomas.

2011-11-21 | E-GEOD-33849 | biostudies-arrayexpress

Expression data from normal thymocytes, 24 day pre-tumor Dnmt3b-deficient thymocytes, Wild-Type Tumors, and Dnmt3b-deficient Tumors

2012-02-22 | E-GEOD-30126 | biostudies-arrayexpress

MicroRNA expression in peripheral T-cell lymphomas

Project description:MicroRNA expression in peripheral T-cell lymphomas

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Methylation and gene expression data from Dnmt3b+/+, Dnmt3b-/- and Dnmt3bCI/CI embryos harvested at E11.5

Project description:Dnmt3b is a DNA methyltransferase, an enzyme which methylates genomic DNA, contributes to genomic stability and transcriptional regulation. Inactivation of Dnmt3b in mice results in embryonic lethality at E13.5. It is however unclear which activities are responsible for this phenomenon. Here, we analyzed methylation and gene expression in Dnmt3b+/+ (WT), Dnmt3b-/- (3bKO) and Dnmt3bCI/CI (3bKI) embryos at E11.5.

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Transcription profiling of human nodal peripheral T-cell lymphomas

Project description:Microarray technology was used to monitor the level of expression of 7,657 human genes in a set of 35 nodal peripheral T-cell lymphomas.

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Genomic Analysis of Peripheral T-Cell Lymphomas

Project description:<p>Peripheral T-cell lymphomas (PTCLs) are a heterogeneous and poorly understood group of non Hodgkin lymphomas. We aim to identify new genetic alterations in PTCL transformation by using a combination of whole exome sequencing of tumor-normal DNA pairs, RNAseq analysis and targeted deep sequencing of candidate genes. Our data identified highly recurrent mutations in epigenetic factors such as TET2, DNMT3A and IDH2 as well as a new highly prevalent mutation in RHOA, the G17V allele that is present in almost 70% of angioimmunoblastic T-cell lymphomas (AITL) and almost 20% of not otherwise specified PTCL (PTCL NOS) samples. In addition, we describe new and recurrent genetic defects including mutations in FYN, ATM, B2M and CD58 implicating SRC signaling, impaired DNA damage response and escape from immune surveillance processes as key players in the pathogenesis of PTCL.</p>

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Increased DNA Methylation of Dnmt3b-Targets Impairs Leukemogenesis (RRBS)

Project description:The de novo DNA methyltransferases Dnmt3a and Dnmt3b are of crucial importance in hematopoietic stem cells, and Dnmt3b has recently been shown to play a role in genic methylation. Forced Dnmt3b expression induced widespread DNA hypermethylation in myc-bcl2 induced leukemias, especially at promoters and gene bodies of stem cell-related genes. MLL-AF9 induced leukemogenesis showed much less pronounced DNA hypermethylation upon Dnmt3b expression. Nonetheless, leukemogenesis was delayed in both models with a shared core set of DNA hypermethylated regions and suppression of stem cell-related genes. Our findings indicate a critical role for Dnmt3b-mediated DNA methylation in leukemia development and maintenance of LSC function. To investigate how Dnmt3b-mediated DNA methylation affects leukemogenesis, we analyzed leukemia development under conditions of high and physiological methylation levels in a tetracycline-inducible knockin mouse model. High expression of Dnmt3b slowed leukemia development in serial transplantations and impaired leukemia stem cell (LSC) function.

2016-01-11 | E-GEOD-71039 | biostudies-arrayexpress

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