Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Changes in mRNA Expression by schedule-dependent combination of 5-FU and selumetinib

ABSTRACT: Anti-tumor effect of the combination between 5-FU and selumetinib was treatment schedule-dependent in BRAF or KRAS mutant CRC cells. Treatment of 5-FU for 2 days followed by selumetinib for another 2 days exhibited synergism for cell viability, whereas single or reversely combined treatment showed antagonism Microarray analysis revealed the distinct groups of genes underlying the efficacy for schedule-dependent treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE89531 | GEO | 2020/12/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Selumetinib

Project description:Selumetinib

| PRJNA712989 | ENA

Homo sapiens

Project description:Changes in mRNA Expression by schedule-dependent combination of 5-FU and selumetinib

| PRJNA352478 | ENA

Selumetinib in adults with NF1 and inoperable plexiform neurofibroma

Project description:The MEK inhibitor selumetinib induces objective responses and provides clinical benefit in children with neurofibromatosis type 1 (NF1) and inoperable plexiform neurofibromas (PNs). To evaluate whether similar outcomes were possible in adult patients, in whom PN growth is generally slower than in pediatric patients, an open-label phase 2 study of selumetinib in adults with NF1 PNs was conducted. Correlative analysis included extraction of RNA followed by sequencing. Samples include paired specimens collected before and on treatment.

2024-10-07 | GSE277520 | GEO

Molecular reprogramming of granulocyte/macrophage progenitor (GMP) clusters upon 5-Fluorouracil (5-FU) treatment

Project description:Single cell RNA Seq and bioinformatic analysis are used to study what processes are important for the molecular reprogramming of GMPs after 5-FU treatment. Samples were collected at different time points (0, 8, 10, 12 and 14 days post treatment)

2017-03-31 | GSE90140 | GEO

FU methane

Project description:FU methane Metagenome

| PRJNA756936 | ENA

5- FU treated organoids

Project description:5-Fluorouracil (5-FU) is a chemotherapeutic drug component that is commonly used for the treatment of solid cancers. The anticancer properties of 5-FU have been attributed to interference with nucleotide synthesis and through direct incorporation into the DNA as being a pyrimidine analog. As both mechanisms of action may have a mutational impact on surviving tumor cells, we performed three independent analyses to characterize the genomic consequences of 5-FU treatment: i) in vitro treatment of intestinal organoids with 5-FU followed by whole genome sequencing, ii) genome-wide mutation analyses in tumor samples from 5-FU treated patients with breast or colorectal cancer, and iii) analysis of paired biopsies from patients treated with 5-FU between biopsies. Our results demonstrate that both in vitro and in vivo 5-FU causes a mutational pattern that is dominated by T>G substitutions in a CTT context and with strong resemblance to COSMIC signature 17. Interestingly, this signature is also found in non 5-FU treated patients, most prominently in esophageal tumors, indicating that distinct endogenous and exogenous triggers can converge into highly similar mutational signatures. Furthermore, our results suggest that 5-FU may have adverse mutagenic effects on healthy cells and contributes to genetic variability in surviving cancer cells thereby contributing to tumor evolution.

| EGAS00001003592 | EGA

miRNA profiling data of mouse bone marrow samples four days post 5-FU treatment versus untreated controls

Project description:To identify miRNAs that regulate hematopoietic response after 5-FU-induced injury, we analyzed miRNA expression changes in bone marrow cells from mice with or without 5-FU treatment. Global miRNA expression profiling of the 5-FU and untreated cohorts showed that 92 miRNAs (among 168 that passed the detection threshold) were significantly upregulated or downregulated, with false discovery rates < 5%. Female 6wk-old C57Bl6/J mice were left untreated or given a single dose of 5-FU (150mg/kg). Four days post treatment whole bone marrow was isolated from each animal (n=3 for treated and n=5 for untreated controls) and lysed for total RNA using Trizol (Invitrogen). Samples were profiled for miRNA expression using a bead-based profiling methodology (Lu et al., 2008). Profiling data were normalized assuming equal total miRNA expression across samples. Differential miRNA expression was analyzed by studentM-bM-^@M-^Ys t-test and then calculated for false discovery rate using the Benjamini and Hochberg method.

2012-09-24 | E-GEOD-39211 | biostudies-arrayexpress

Transcription profiling of human HCT116 parental cells treated with 5-FU or SN38 and non-treated parental cells, 5-FU resistant and SN39 resistant cells

Project description:The transcriptional profiles of the HCT116 parental cells following treatment with either 5-FU or SN38 for 24h were assessed. In addition, basal comparisons between HCT116 parental and HCT116 5-FU -resistant and HCT116 SN38-resistant cells were also assessed.

2009-03-30 | E-MEXP-1691 | biostudies-arrayexpress

Epigenetic and genetic change through cell cycling under selumetinib treatment

Project description:Here we apply single cell bisulfite sequencing to detect epigenetic and genetic changes that occur in BRAF V600E cells that escape G1 arrest and return to the cell cycle during treatment with the MEK inhibitor selumetinib. We detect no major changes in DNA methylation, but find that cells in G2 are enriched in large amplifications and deletions that we ascribe to abnormal mitotic chromosome segregation.

2022-09-11 | GSE212899 | GEO

Copy number analysis of selumetinib-resistant CRC cells lines

Project description:Copy number analysis to compare parental colorectal cancer cell lines and their selumetinib-resistant derivatives and identify gene copy changes that might contribute to resistance

2019-03-11 | GSE126367 | GEO

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