Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of human neuroblastoma cell lines treated with ALKAL2 and/or lorlatinib

ABSTRACT: RNA-seq of human neuroblastoma cell lines treated with ALKAL2 and/or lorlatinib

PROVIDER: PRJEB40483 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR4619060_1.fastq.gz	Fastqsanger.gz
	ERR4619060_2.fastq.gz	Fastqsanger.gz
	ERR4619070_1.fastq.gz	Fastqsanger.gz
	ERR4619070_2.fastq.gz	Fastqsanger.gz
	ERR4619080_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 120

Similar Datasets

Human neuroblastoma cell lines: control vs treated with verlindamycin and ATRA

Project description:Human neuroblastoma cell lines: control vs treated with verlindamycin and ATRA

| PRJNA741476 | ENA

RNA-seq of GSK-J4 Treated Neuroblastoma Cell Lines

Project description:RNA-seq of GSK-J4 Treated Neuroblastoma Cell Lines

| PRJNA434379 | ENA

RNA expression analysis of neuroblastoma cell lines treated with epigenetic drugs

Project description:The impact of drugs inhibiting DNA methylation (5-aza-2'-deoxycytodine, DAC) and EZH2 (EPZ-6438) on the neuroblastoma transcriptome was analyzed in two neuroblastoma cell lines. Parallel analyses investigated associated changes in histone modification and DNA methylation. The neuroblastoma cell lines Be(2)-C and IMR5-75 were treated with DAC and EPZ-6438 in combination or alone. Controls were treated with solvent (DMSO). RNA was isolated and sequenced.

2016-09-08 | E-GEOD-79859 | biostudies-arrayexpress

RNA-seq of human neuroblastoma cell lines treated with the ATR inhibitor BAY 1895344

Project description:RNA-seq of human neuroblastoma cell lines treated with the ATR inhibitor BAY 1895344

| PRJEB45783 | ENA

Kinome reprogramming of G2/M kinases and repression of MYCN contribute to superior efficacy of lorlatinib in ALK-driven neuroblastoma

Project description:Mutations in the tyrosine kinase domain of the Anaplastic Lymphoma Kinase (ALK) oncogene in neuroblastoma occur most frequently at one of three hotspot amino acid residues, with the F1174* and F1245* variants conferring de novo resistance to first and second generation ALK inhibitors including crizotinib and ceritinib. Lorlatinib, a third generation ALK/ROS inhibitor, overcomes de novo resistance and induces complete tumor regressions in patient-derived xenograft (PDX) models unresponsive to crizotinib. Lorlatinib has now completed Phase 1 testing in children and adults with relapsed/refractory ALK-driven neuroblastoma, and entered pivotal Phase 3 testing within the Children’s Oncology Group. To define mechanisms underlying the superior activity of lorlatinib, we utilized a chemical proteomics approach to quantitatively measure functional kinome dynamics in response to the ALK inhibitors lorlatinib and crizotinib, in clinically relevant ALK-driven neuroblastoma PDX models. Lorlatinib was a markedly more potent inhibitor of ALK and preferentially downregulated several kinases implicated in G2/M cell cycle transition compared to crizotinib. Lorlatinib treatment also led to the repression of MYCN expression and its occupancy at promoters of the same G2/M kinases. These data providing mechanistic insight in neuroblastoma into the far improved efficacy of lorlatinib over crizotinib for the treatment of ALK-driven neuroblastoma.

2024-07-29 | GSE273349 | GEO

Neuroblastoma cell lines

Project description:Neuroblastoma cell lines

| PRJEB6889 | ENA

Neuroblastoma cell lines

Project description:Neuroblastoma cell lines

| PRJNA515054 | ENA

RNA-seq of human neuroblastoma cell lines treated with ALKAL2 and/or lorlatinib

Project description:ALK is a tyrosine kinase receptor and oncogene in neuroblastoma (NB). The receptor is activated by the ALKAL2 ligand, but it is unknown whether missregulation of this ligand may play a role in NB carcinogenesis. To characterize the transcriptomic response to ALKAL2 in neuroblastoma cell lines, RNA-Seq was performed on NB1 and IMR32 human NB cell lines.

2020-11-24 | E-MTAB-9598 | biostudies-arrayexpress

Transcriptomic profiling of three different neuroblastoma cell lines (CLB-BAR, CLB-GE and SK-N-AS) in response to ALK inhibition

Project description:Anaplastic Lymphoma Kinase (ALK) is a tyrosine kinase receptor which is a clinical target of major interest in cancer, including neuroblastoma. To better understand ALK signaling, three different neuroblastoma cell lines (CLB-BAR, CLB-GE and SK-N-AS) were cultured for 1hr and 24hrs in control conditions or after treatment with the ALK inhibitors crizotinib or lorlatinib. RNA-Seq experiments were performed to determine the expression changes resulting from ALK inhibition. Together with parallel phosphoproteomic experiments, these data unveil several important conserved oncogenic pathways in neuroblastoma.

2018-09-01 | E-MTAB-6654 | biostudies-arrayexpress

Phosphoroteomics analysis of ALK signaling in neuroblastoma cells

Project description:We used mass spectrometry-based proteomics to unravel anaplastic lymphoma kinase (ALK) signaling in the ALK and MYCN amplified neuroblastoma cell line, NB1. We specifically measured the ALK phosphoproteome upon siRNA depletion of ALK and upon ALK inhibition using the ALK-targeting small-molecule inhibitor lorlatinib. For quantitative phosphoproteomics we used a tandem mass tag (TMT)-based approach. Conditions for the TMT 11-plex setup is specified below. For each siRNA depletion experiment, NB1 cells were treated with siRNA (80 nM; as specified below) for 48 hours prior to stimulation with 0.1% DMSO for 30 minutes. For inhibitor treatment, NB1 cells were treated for 30 minutes with either 10 microM or 10 nM lorlatinib. The experimental treatment conditions and TMT11-plex labeling are specified below: 126: siControl replicate 1, 0.1% DMSO 127N: siControl replicate 2, 0.1% DMSO 127C: siControl replicate 3, 0.1% DMSO 128N: siALK sequence 1, 0.1% DMSO 128C: siALK sequence 2, 0.1% DMSO 129N: siALK mix of sequence 1 and 2, 0.1% DMSO 129C: 10 microM lorlatinib replicate 1 130N: 10 microM lorlatinib replicate 2 130C: 10 microM lorlatinib replicate 3 131N: 10 nM lorlatinib replicate 1 131C: 10 nM lorlatinib replicate 2

2018-11-21 | PXD009477 | Pride

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