Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

DNA methylation profiling of lung adenocarcinomas and patient-matched non-malignant lung

ABSTRACT: Gene function in cancer is often cell type-specific. The epithelial cell-specific transcription factor ELF3 is a documented tumour suppressor in many epithelial tumours yet displays oncogenic properties in others. Here, we show that ELF3 is an oncogene in the adenocarcinoma subtype of lung cancer (LUAD), providing genetic, functional, and clinical evidence of subtype specificity. We discover a region of focal amplification at chromosome 1q32.1 encompassing the ELF3 locus in LUAD which is absent in the squamous subtype. Gene dosage and promoter hypomethylation affect the locus in up to 80% of LUAD analysed. ELF3 expression was required for tumour growth and a pan-cancer expression network analysis supports its subtype and tissue specificity. We further show that ELF3 displays strong prognostic value in LUAD but not LUSC. We conclude that, contrary to many other tumours of epithelial origin, ELF3 is an oncogene and putative therapeutic target in LUAD.

ORGANISM(S): Homo sapiens

PROVIDER: GSE139032 | GEO | 2019/10/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Expression profiling of isogenic A549 cell lines with and without ELF3 knock-down

Project description:Gene function in cancer is often cell type-specific. The epithelial cell-specific transcription factor ELF3 is a documented tumour suppressor in many epithelial tumours yet displays oncogenic properties in others. Here, we show that ELF3 is an oncogene in the adenocarcinoma subtype of lung cancer (LUAD), providing genetic, functional, and clinical evidence of subtype specificity. We discover a region of focal amplification at chromosome 1q32.1 encompassing the ELF3 locus in LUAD which is absent in the squamous subtype. Gene dosage and promoter hypomethylation affect the locus in up to 80% of LUAD analysed. ELF3 expression was required for tumour growth and a pan-cancer expression network analysis supports its subtype and tissue specificity. We further show that ELF3 displays strong prognostic value in LUAD but not LUSC. We conclude that, contrary to many other tumours of epithelial origin, ELF3 is an oncogene and putative therapeutic target in LUAD.

2019-10-23 | GSE137479 | GEO

DNA copy number profiling of lung adenocarcinomas and patient-matched non-malignant lung

2019-10-23 | GSE139294 | GEO

Club cells employ regeneration mechanisms during lung tumorigenesis

Project description:Lung adenocarcinoma (LUAD) is one of the deadliest malignancies worldwide. Dynamic lineage changes within the lung epithelium and the high plasticity of these epithelial cells confound the correct identification of the cell-of-origin of LUAD. Here, we combined lineage-tracing mouse models with an autochthonous cell type-independent LUAD model in order to discover the cellular origin of ALK-translocated LUAD. We identified Club and AT2 cells as the cells-of-origin of LUAD. Moreover, we uncovered epigenetic imprints in the tumours originating from Club or AT2 cells by whole-genome bisulfite sequencing. Single-cell transcriptomes of Club cells at different stages of tumour development identified two trajectories of Club cell evolution. On both routes, tumours lose their Club cell identity and gain an AT2-like phenotype. Together, this study highlights the role of Club cells in LUAD initiation and unveils key mechanisms conferring LUAD heterogeneity.

2022-06-30 | GSE176185 | GEO

Club cells employ regeneration mechanisms during lung tumorigenesis

2022-06-30 | GSE176184 | GEO

Epithelial Tumour Suppressor ELF3 is a Lineage-Specific Amplified Oncogene in Lung Adenocarcinoma

Project description:Epithelial Tumour Suppressor ELF3 is a Lineage-Specific Amplified Oncogene in Lung Adenocarcinoma

| PRJNA565706 | ENA

Project description:Epithelial Tumour Suppressor ELF3 is a Lineage-Specific Amplified Oncogene in Lung Adenocarcinoma

| PRJNA563664 | ENA

Amplification of 1q32.1 refines the molecular classification of endometrial carcinoma: SNP array

Project description:The experiment aimed at refining the classification of endometrial cancer by profiling somatic copy number aberrations (SCNAs). SCNAs affecting chromosome 1q32.1 significantly correlated with worse survival and functional validation of a plausible oncogene showed MDM4 as an oncogenic driver in 1q32.1 and a putative therapeutic target for NSMP ECs.

2019-07-27 | E-MTAB-5908 | biostudies-arrayexpress

Identification of a cancer driver lncRNA in DNA damage response

Project description:We report that the lncRNA SCAT7 (ELF3-AS1) is involved in the activation of the DNA damage response in cisplatin resistant LUAD cells, akin cisplatin in sensitive cells. Therefore SCAT7 is a potential therapeutic target for drug resistant cancers

2021-01-06 | GSE116192 | GEO

An Organoid Biobank for Childhood Kidney Cancers that Captures Disease and Tissue Heterogeneity

Project description:Kidney tumours are among the most common solid tumours in children, comprising several distinct subtypes differing in many aspects, including cell-of-origin, genetics, and pathology. Pre-clinical cell models capturing the disease heterogeneity are currently lacking. Here, we describe the first paediatric cancer organoid biobank. It contains tumour and matching normal kidney organoids from over 50 children with different subtypes of kidney cancer, including Wilms tumours, malignant rhabdoid tumours, renal cell carcinomas, and congenital mesoblastic nephromas. The malignant rhabdoid tumour organoids represent the first organoid model for tumours of non-epithelial origin. The tumour organoids retain key properties of native tumours, useful for revealing patient-specific drug vulnerabilities. We further demonstrate that organoid cultures derived from Wilms tumours consist of multiple different cell types, including epithelial, stromal and blastemal-like. Our organoid biobank captures the cellular heterogeneity of paediatric kidney tumours, providing a representative collection of well-characterized models for basic cancer research, drug-screening, and personalized medicine.

2019-09-18 | GSE137544 | GEO

Development of gene expression profiles for murine breast tumours overexpression the transcription factor PRH

Project description:In order to establish a profile of gene expression of tumours overexpressing PRH we performed agilient microarray analysis on four 4T1 tumour samples engineered to overexpress PRH, and four control tumours with normal PRH expression. cancer, colorectal metastasis to the liver and matched healthy tissues. The tumours had recieved no treatement prior to resection. The expression profiles were compared by one colour microarray analysis between PRH overexpression and control tumours. Genes consistently differentially expressed between the groups were taken forward for further analysis. Preparation of the tumours: 4T1 cells were infected with Adenoviral-PRH or empty Adenovirus at MOI 50 for 24 hrs. Adenoviral constructs described in Kershaw, R.M., et al., PRH/HHex inhibits the migration of breast and prostate epithelial cells through direct transcriptional regulation of Endoglin. Oncogene, 2014. 33(49): p. 5592-600. Cells were washed 4x with PBS, trypsinised, washed and resuspended in Opti-memï£¨ (Invitrogen) at 1.25x106 cells/ml and kept on ice for 20-30 min before injection. Aliquots 200 Î¼l / 2.5x105 of the cells were injected into the no. 3 fat pad of 6-8 week old female BALB/C mice. Total RNA was extracted from each tumour using the Qiagen miRNAeasy kit, processed into cRNA using the Agilient low input, one colour labelling kit, hybridised onto the 8 x 66k whole human genome expression microarrays. Data was normalised in R64 and comparison matrices between matched Tumour and Healthy endothelum were constructed. Genes upregualated in all the comparisons were taken forward for further analysis.

2016-06-15 | E-GEOD-83319 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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