Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The Genetic and Epigenetic Features of Bilateral Wilms Tumor Predisposition [DNA methylation]

ABSTRACT: The Genetic and Epigenetic Features of Bilateral Wilms Tumor Predisposition [DNA methylation]

PROVIDER: PRJNA939213 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

The Genetic and Epigenetic Features of Bilateral Wilms Tumor Predisposition

Project description:The Genetic and Epigenetic Features of Bilateral Wilms Tumor Predisposition

| PRJNA940412 | ENA

The Genetic and Epigenetic Features of Bilateral Wilms Tumor Predisposition [RNA-Seq]

Project description:The Genetic and Epigenetic Features of Bilateral Wilms Tumor Predisposition [RNA-Seq]

| PRJNA940419 | ENA

The Genetic and Epigenetic Features of Bilateral Wilms Tumor Predisposition [RNA-Seq]

Project description:This study comprehensively evaluated the landscape of genetic and epigenetic events that predispose to synchronous bilateral Wilms tumor (BWT). We performed whole exome or whole genome sequencing, total-strand RNA-seq, and DNA methylation analysis using germline and/or tumor samples from 68 patients with BWT from St. Jude Children’s Research Hospital and the Children’s Oncology Group.

2023-11-10 | GSE226478 | GEO

The Genetic and Epigenetic Features of Bilateral Wilms Tumor Predisposition [DNA methylation]

2023-11-10 | GSE226234 | GEO

The Genetic and Epigenetic Features of Bilateral Wilms Tumor Predisposition

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-11-09 | GSE226480 | GEO

Project description:The Genetic and Epigenetic Features of Bilateral Wilms Tumor Predisposition

| PRJNA943166 | ENA

Germline Variant in Ctcf Links Mental Retardation to Wilms Tumor Predisposition

Project description:SNP arrays was combined with next generation sequencing (NGS) to identify an LOH in 16q together with an unreported CTCF missense variant in its zinc finger domain. CTCF is within 16q LOH. We found that germline heterozygous variant I446K became homozygous in the tumor due to a loss of heterozygosity rearrangement affecting the whole q arm on chromosome 16. Based on CTCF role in regulating the epigenetic architechture of the genome, our findings reveal CTCF variant I446K as a link between MRD21 and Wilms tumor predisposition.

2022-01-11 | GSE193233 | GEO

Germline Variant in *Ctcf* Links Mental Retardation to Wilms Tumor Predisposition

Project description:Germline Variant in *Ctcf* Links Mental Retardation to Wilms Tumor Predisposition

| PRJNA795462 | ENA

Germline Variant in Ctcf Links Mental Retardation to Wilms Tumor Predisposition

Project description:Germline Variant in Ctcf Links Mental Retardation to Wilms Tumor Predisposition

| PRJNA795463 | ENA

Wilms Tumor cells with WT1 mutations have characteristic features of mesenchymal stem cells

Project description:Wilms tumors are genetically heterogeneous kidney tumors whose cells of origin are unknown. Tumors with WT1 mutations and concomitant loss of the wild-type allele represent a distinct subgroup, frequently associated with mutations in CTNNB1. Here we describe the establishment and characterization of long-term cell cultures derived from five individual Wilms tumors with WT1 mutations. Three of these tumor cell lines also had CTNNB1 mutations and an activated canonical Wnt signaling pathway as measured by β-catenin/TCF transcriptional activity. Four of the five Wilms cell lines had a stable normal karyotype for at least 25 passages, and four lines showed loss of heterozygosity of chromosome 11p due to mitotic recombination in 11p11. Gene expression profiling revealed that the Wilms tumor cell lines are highly similar to human mesenchymal stem cells (MSCs) and FACS analysis demonstrated expression of MSC-specific surface proteins CD105, CD90 and CD73. The stem cell like nature of the Wilms tumor cells is further supported by their adipogenic, chondrogenic, osteogenic and myogenic differentiation potentials. By generating multipotent mesenchymal precursors from paraxial mesoderm (PAM) in tissue culture using embryonal stem cells, gene expression profiles of PAM and MSCs were described. Using these published gene sets we found coexpression of a large number of genes in Wilms tumor cell lines, PAM and MSCs. Lineage plasticity is indicated by the simultaneous expression of genes from the mesendodermal and neuroectodermal lineages. We conclude that Wilms tumors with WT1 mutations have specific traits of PAM, which is the source of kidney stromal cells.

2010-02-01 | GSE18058 | 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