Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic analysis of HES induced [E(spl)mγ and dpn; DM] Drosophila larval primary CNS tumours vs HES allograft tumours in w1118 host flies

ABSTRACT: The goal of this project was to compare NGS derived transciptional profiles of primary larval CNS tumours and allograft tumours from two stages (first-T0 and forth-T3) in Drosophila that are induced by overactivation of two HES genes [E(spl)mγ and dpn;DM] in order to decipher if these two Hes genes control similar or different sets of genes as primary hypeplasias transition to malignant tumours. The results of this study show that overactivation of DM continues to negatively regulate neuronal differentiation genes as the DM hyperplasias become more malignant and that genes related to stress and metabolsim are upregulated

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE179507 | GEO | 2021/09/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptomic analysis of HES induced [E(spl)mγ and dpn DM] Drosophila larval primary CNS tumours vs HES allograft tumours in w1118 host flies

Project description:Transcriptomic analysis of HES induced [E(spl)mγ and dpn DM] Drosophila larval primary CNS tumours vs HES allograft tumours in w1118 host flies

| PRJNA744081 | ENA

Transcriptomic analysis of Notch (N) induced [NΔecd] Drosophila larval primary CNS tumours vs N allograft tumours in w1118 host flies

Project description:The goal of this project was to compare NGS derived transciptional profiles of primary larval CNS tumours and allograft tumours from two stages (first-T0 and forth-T3) in Drosophila that are induced by overactivation of N pathway in order to decipher if N regulates similar or different sets of genes as primary hypeplasias transition to malignant tumours. The results of this study show that overactivation of N negatively regulates genes related to neuronal differentiation processes genes as N hyperplasias become more malignant and that genes related to stress, metabolsim and immunity are upregulated

2023-05-30 | GSE219067 | GEO

Comparison of gene expression data between undifferentiated hES cells and MSC-derived hES cells

Project description:Analysis of genes that were differentially expressed in MSC-derived hES cells (VUB01 and SA01) as compared to VUB01 and SA01 undifferentiated hES cells Keywords: differentiation state analysis

2008-05-20 | GSE7879 | GEO

Transcriptomic dysregulation in aggressive and malignant prolactin tumours

Project description:Pituitary tumours are generally benign. However, many are invasive and some of these are aggressive with high proliferation and recurrence rates. Only metastatic tumours are considered malignant and are rare (0.2%). To identify molecular events associated with the aggressive and malignant phenotypes, we combined a comparative genomic hybridization and transcriptomic analysis of 13 prolactin (PRL) tumours classified as non-invasive (NI; n=5), invasive (I; n=2) or aggressive-invasive (AI; n=6). Each tumour showed copy number alterations which appeared to be varied and discrete in the NI and I tumour groups, and more numerous and extensive in the AI tumour group. Allelic loss within the p arm region of chromosome 11 was detected in five of the AI tumours. This region contains the cytobands 11p15.2, 11p15.1, 11p14.3, 11p14.2, 11p14.1, 11p13, 11p12 and 11p11.2. Furthermore, an allelic loss in the 11q arm was also observed in three of these five tumours, which were considered malignant based on the presence of metastases. The comparison of genomic and transcriptomic data showed that allelic loss impacted upon the expression of genes located in the imbalanced region. An original data filtering strategy allowed us to highlight five genes (DGKZ, CD44, TSG101, GTF2H1 and HTATIP2), within the missing 11p region, potentially responsible for triggering the aggressive and malignant phenotypes of PRL tumours. Our novel combined genomic and transcriptomic analysis underlines the importance of chromosome 11 allelic loss in aggressive and malignant PRL tumours and led us to propose a new strategy to find markers of progression in rare tumours.

2011-03-16 | GSE22812 | GEO

Transcription profiling of human hES cells and MSC-derived hES cells

2008-06-20 | E-GEOD-7879 | biostudies-arrayexpress

Transcriptomic dysregulation in aggressive and malignant prolactin tumours

2011-03-16 | E-GEOD-22812 | biostudies-arrayexpress

Hes mediated transcriptomics in Drosophila larval CNS

Project description:Excessive activation of Hes causes stem cell hyperplasia in larval CNS. Transcriptomics of Notch induced hyperplasia and Hes induced hyperplasia were compared Using affymetrix microarray, global gene expression analysis was performed.

2020-11-03 | GSE141793 | GEO

Methylation profiling of Malignant Rhabdoid Tumours

Project description:An observational experiment to methylation profile 79 SMARCB1 negative primary tumours from patients diagnosed with Malignant Rhabdoid Tumours.

2020-07-15 | E-MTAB-6708 | biostudies-arrayexpress

Analysis of circulating microRNAs in adrenocortical tumours

Project description:Differential diagnosis of adrenocortical adenoma and carcinoma is of pivotal clinical relevance, as the prognosis and clinical management of benign and malignant adrenocortical tumours is entirely different. Circulating microRNAs are promising biomarker candidates of malignancy in several tumours. In the present study we investigate circulating microRNAs in adrenocortical tumours and to evaluate their potential applicability as biomarkers of malignancy.

2013-11-19 | GSE49674 | GEO

RNA-seq profiling of Malignant Rhabdoid Tumours

Project description:An observational experiment to methylation profile 23 SMARCB1 negative primary tumours from patients diagnosed with Malignant Rhabdoid Tumours.

2024-12-31 | E-MTAB-6775 | 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