Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Hypomethylating agents sensitize diffuse large B-cell lymphoma to venetoclax

ABSTRACT: Hypomethylating agents sensitize diffuse large B-cell lymphoma to venetoclax

PROVIDER: PRJNA926939 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Hypomethylating agents sensitize diffuse large B-cell lymphoma to venetoclax

Project description:We established acquired venetoclax resistant OCI-LY1R cell line by treating venetoclax sensitive parental OCI-Ly1 cell line with increasing doses of venetoclax up till 1µM. Parental OCI-Ly1 and venetoiclax-resistant OCI-Ly1R cells were treated with vehicle control or decitabine at 1uM for 3 days. We found that decitabine differantially regulated gene expression in venetoclax sensitive and resistant cells. With gene set enrichment analysis, we identified two pathways that were deregulated by decitabine in both cell lines.

2023-07-25 | GSE223598 | GEO

thermal proteome profiling of hypomethylating agents in infant ALL

Project description:thermal proteome profiling of hypomethylating agents in infant ALL for elucidation of their mode of action.

2022-11-15 | PXD030539 | Pride

Comparing gene expression in ABT-199 (venetoclax) sensitive and resistant diffuse large B cell lymphoma cell (DLBCL) lines

Project description:RNA-sequencing was performed to evaluate gene expression changes between ABT-199 (venetoclax) sensitive and resistant matched diffuse large B cell lymphoma cell lines

2024-06-20 | GSE252306 | GEO

SETD2 loss sensitizes kidney cancer cells to DNA hypomethylating agents

Project description:SETD2 loss sensitizes kidney cancer cells to DNA hypomethylating agents

| PRJNA927290 | ENA

SETD2 loss sensitizes kidney cancer cells to DNA hypomethylating agents

Project description:Large-scale sequencing efforts in Clear cell renal cell carcinoma (ccRCC) have found a high prevalence of mutations in chromatin-related genes. Prominent within this group is SETD2, which is mutated in 15% of ccRCC and is associated with aggressive disease. SETD2 is a methyltransferase responsible for trimethylating lysine 36 on histone H3 (H3K36me3). Although it is not completely understood how SETD2 loss contributes to ccRCC tumorigenesis, it is thought that it reprograms the epigenetic landscape of the cell. Here we explore the impact that SETD2/H3K36me3 loss has on the DNA methylome in ccRCC cells. DNA methylation was measured using the EPIC DNA methylation assay in 786-O ccRCC cells and non-cancerous transformed proximal tubule kidney cells (HKC) with and without SETD2. Sensitivity to DNA hypomethylating agents was assessed by dose-response assay using 5-aza-2'-deoxycytidine. Apoptosis was measured via Annexin-V/PI staining by flow cytometry. Mitochondrial fitness was evaluated by electron microscopy and flow cytometry. Moreover, activity of 5-aza-2'-deoxycytidine, a DNA hypomethylating agent, in was assessed in SETD2 WT/KO xenografts in NOD-Scid mice. SETD2 loss resulted in DNA hypermethylation in HKC cells and to a greater extent in 786-O. Dose-response assays showed that SETD2-null ccRCC cells are sensitive to 5-aza-2'-deoxycytidine. Furthermore, Annexin-V/PI staining revealed more apoptotic and necrotic cells in SETD2-null cells following 5-aza-2'-deoxycytidine treatment, which was rescued using a Caspase inhibitor. In addition, 5-aza-2'-deoxycytidine induced profound changes in mitochondria in SETD2-null cells, including loss of membrane potential and size reduction. Indeed, in vivo experiments verified increased SETD2-null xenografts’ sensitivity to 5-aza-2'-deoxycytidine. We show that SETD2 loss in ccRCC cells causes DNA hypermethylation, creating a synthetic lethal dependency with DNA hypomethylating agents.

2024-07-01 | GSE223688 | GEO

Venetoclax cooperates with ionizing radiation to attenuate Diffuse Midline Glioma tumor growth

Project description:This article highlights the radiation induced cytotoxic effect of the BCL2 inhibitor, venetoclax, in diffuse midline gliomas (DMG). 1. RNA-seq: We performed bulk RNA sequencing of DMG cells exposed to 6Gy radiation and found the genes upregulated after radiation compared to unirradiated controls. 2. DNA Repair shRNA screen: We also performed a DNA Repair shRNA screen and identified the genes which are responsible for radioresistance in DMG.

2022-03-23 | GSE198979 | GEO

SETD2 loss sensitizes kidney cancer cells to DNA hypomethylating agents [methylation]

Project description:SETD2 loss sensitizes kidney cancer cells to DNA hypomethylating agents [methylation]

| PRJNA927301 | ENA

DNA hypomethylating agents increase activation and cytolytic activity of CD8+ T-cells

Project description:DNA hypomethylating agents increase activation and cytolytic activity of CD8+ T-cells

| PRJNA637641 | ENA

Targeting SUMOylation sensitizes Acute myeloid leukemia to Venetoclax treatment

Project description:Acute myeloid leukemia (AML) is a hematopoietic cancer characterized by the proliferation and accumulation of aberrant immature myeloid progenitor blasts in bone marrow and peripheral blood. Venetoclax (VEN), a selective B-cell lymphoma 2 (BCL-2) inhibitor, has received FDA approval for AML treatment in combination with hypomethylating agents (HMA). However, treatment failure and therapy resistance present an urgent need for new therapies to overcome VEN resistance and enhance VEN efficacy. We propose inhibition of SUMOylation as a novel therapy with the potential to address this need. SUMOylation regulates protein function by covalently attaching Small Ubiquitin-like MOdifier (SUMO) proteins to target proteins via an enzymatic cascade. Our study aims to evaluate the effects of SUMOylation inhibition on anti-AML activity of VEN and dissert the underlying mechanism.

2024-05-27 | GSE267885 | GEO

Venetoclax cooperates with ionizing radiation to attenuate Diffuse Midline Glioma tumor growth

Project description:Venetoclax cooperates with ionizing radiation to attenuate Diffuse Midline Glioma tumor growth

| PRJNA817612 | ENA