Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of FL-Fc-DM1 drug on gene expression of THP-1 cells pretreated with cytarabine.

ABSTRACT: Cytarabine is one of the first line chemo drugs to treat acute myeloid leukemia (AML). However, cytarabine can induce AML cell cell cycle arrest at G0/G1 phase. These cell-cycle-arrested AML cells resist cytarabine, show a senescence-like phenotype or stem-cell like phenotype. To eliminate these cell-cycle arrested cells, we developed a FL-Fc-DM1 drug by conjugating FLT3 liangd Fc fusion protein and mertansine. We used the THP-1 cells as a AML model. The total mRNA of THP-1 cells treated with different drugs (cytarabine, FL-Fc-DM1, FL-Fc) were sequenced.

ORGANISM(S): Homo sapiens

PROVIDER: GSE270338 | GEO | 2024/06/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Shared Molecules

Only show the datasets with similarity scores above: 0.5

Threshold

0.5

Similar Datasets

Effect of FL-Fc-DM1 drug on gene expression of THP-1 cells pretreated with cytarabine.

Project description:Effect of FL-Fc-DM1 drug on gene expression of THP-1 cells pretreated with cytarabine.

| PRJNA1126229 | ENA

Differential gene expression analysis of pediatric acute myeloid leukemia cell lines treated with azacytidine and panobinostat alone or in combination and compared to vehicle treated cells.

Project description:Pediatric AML cell lines (MV4;11, AML-193 and THP-1) were treated with DNA hypomethylating agent (azacytidine) and a pan histone deactylase inhibitor (panobinostat) alone or in combination. Treatment of AML cell lines with these epigenetic drugs synergistically suppresses cell viability in vitro and in xenograft models in vivo. Data show differential regulation of gene expression in AML cell lines by epigenetic drugs at concentrations which retained cell viability at a minimum of 75% even in the combination treatment.

2017-07-01 | GSE83983 | GEO

Posttranslational splicing modifications as a key mechanism in cytarabine resistance in AML

Project description:Despite the approval of several drugs for AML, cytarabine is still widely used as a therapeutic approach. However, most patients show resistance and only 10% of them overcome the disease. Using high-throughput screening analysis, we show that phosphorylation levels of SR proteins were elevated during cytarabine resistance. Moreover, phosphorylation of SR proteins at diagnosis was different between responder and non-responder patients, pointing to their utility to predict response. These changes correlated with altered transcriptomic profiles of SR protein target genes.

2023-07-04 | PXD034010 | Pride

Metabolomics Workbench ST000288 - GNPS - Metabolomic profiling of AML Cell Lines

Project description:In vitro study with AML cell lines that are treated with different concentrations of cytarabine (nucleoside analog). 8 AML cell lines were incubated for 24hr with 0uM, 1uM and 10uM ara-C. After 24hr the cells were washed and pellets were stored in -80°C for genomic and metabolomic analysis.

2018-08-02 | MSV000082685 | GNPS

Metabolomic profiling of AML Cell Lines

2015-02-15 | ST000288 | MetabolomicsWorkbench

Gene expression changes in SHI-1 cells following exposure to disulfiram/copper, niclosamde or combined drugs

Project description:Disulfiram and niclosamide were identified as drugs that induced depletion of an MLL-AF9-luciferase fusion protein in THP-1 AML cells, in a bioluminescence sreen. MLL-fusion protein depletion was confirmed in AML and ALL cell lines expressing different MLL-fusion proteins. Combination of disulfiram with niclosamide was found to enhance depletion of MLL-fusion proteins. To investigate whether this enhanced depletion resulted in increased suppression of downstream target genes. MLL-AF6 expressing SHI-1 cells were exposed to disulfiram/copper, nciclosamide or combined drugs. SHI-1 cells were treated for 16 hours with 0.3uM disulfiram / 1uM copper, 5uM niclosamide or combined drugs and RNAseq performed on isolated RNA.

2024-07-03 | GSE262673 | GEO

Exploring the cytotoxic effects of dBET1 on multiple molecular subtypes of Acute myeloid leukemia cells

Project description:Acute myeloid leukemia (AML) represents an aggressive hematopoietic malignancy with a prognosis inferior to that of other leukemias. Recent targeted therapies offer new opportunities to achieve better treatment outcomes. However, due to the complex heterogeneity of AML, its prognosis is remain dismal. In this study, we first identified the correlation between high expression of BRD4 and overall survival of AML patients. Targeted degradation of BRD2, BRD3, and BRD4 proteins by dBET1, a PROTAC against BET family members, showed cytotoxic effects on Kasumi (AML1-ETO), NB4 (PML-RARa), THP-1 (MLL-AF9), and MV4-11 (MLL-AF4) AML cell lines representing different molecular subtypes of AML. Furthermore, we determined that dBET1 treatment arrested cell cycling and enhanced apoptosis and c-MYC as the downstream target. Collectively, our results indicated that dBET1 has broad cytotoxic effects on AML cells with different molecular lesions and provide more benefits to AML patients.

2022-06-27 | GSE196693 | GEO

Adverse stem cell features in a single AML sample predict clinical outcome in AML patient cohorts

Project description:Patients with acute myeloid leukemia (AML) suffer dismal prognosis and the most adverse subpopulation within each tumor determines patient’s prognosis. To better understand challenging features in AML, we studied individual stem cells from a single AML sample, complementing genomic with in vivo functional studies. Primary tumor cells from an AML patient’s first and second relapse were transplanted into NSG mice to establish serially transplantable patient derived xenografts (PDX). In an innovative approach, twelve derivative PDX clones were generated thereof, each derived from a single AML stem cell as proven by molecular barcoding, and were color-marked to facilitate multiplex competitive in vivo assays. PDX clones consisted of four different genomic clusters; one cluster displayed resistance against Cytarabine treatment, while two other clusters harbored increased stem cell potential, indicating that stemness and treatment resistance had evolved independently in the sample. In vivo functional data correlated closely with the phylogenetic tree calculated from exome data. The Cytarabine-resistant cluster was characterized by a distinct gene expression profile, and a score thereof predicted outcome in large clinical patient data cohorts. Taken together, we provide proof of concept that intra-sample heterogeneity mimics inter-sample heterogeneity in AML. Stem cell disparities within a single sample allow insights into adverse characteristics of general importance for AML.

2022-04-04 | PXD026296 | Pride

Genome-wide CRISPR screening identifies the E3 ubiquitin ligase HERC1 as a modulator of the response to nucleoside analogs in acute myeloid leukemia

Project description:We identified the Ubiquitin Ligase HERC1 in the context of cytarabine response in a genome-wide CRISPR screen in murine AML. We hypothesized to detect early transciptomic changes in cytarabine treated murine AML cells genetically targeted by using single guide RNAs targeting HERC1 and Non-targeting Control.

2024-08-02 | GSE273667 | GEO

Notch Pathway Activation Targets AML Cell Homeostasis and Differentiation: THP1 cell line

Project description:Expression data from untreated or Dll4-Fc treated THP1 cell line. We used Dll4-Fc stimulation of AML cells to study whether Notch activation has an impact on AML. We analyzed THP1 cell line in vitro treated with Dll4-Fc or vehicle control to determine genes affected by Notch activation. THP1 cell line was cultured on plate coated with 30 nM Dll4-Fc or vehicle for 48 hours prior to RNA extraction and hybridization to Human Genome U133 Plus 2.0 Affymetrix arrays.

2013-01-18 | E-GEOD-42259 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data