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Chromatin Analysis of Wilms Tumor Highlights Stem Cell Properties and a Renal Developmental Network

ABSTRACT: Wilms tumors are pediatric cancers thought to arise from kidney-specific stem cells. In order to identify transcriptional and epigenetic mechanisms that drive these malignant cells, we compared genomewide chromatin profiles of Wilms tumors to embryonic stem (ES) cells and normal kidney.

ORGANISM(S): Homo sapiens

PROVIDER: GSE20512 | GEO | 2010/05/05

SECONDARY ACCESSION(S): PRJNA125231

REPOSITORIES: GEO

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Chromatin Analysis of Wilms Tumor Highlights Stem Cell Properties and a Renal Developmental Network

Project description:Wilms tumors are pediatric cancers thought to arise from kidney-specific stem cells. In order to identify transcriptional and epigenetic mechanisms that drive these malignant cells, we compared genomewide chromatin profiles of Wilms tumors to embryonic stem (ES) cells and normal kidney. Data represent examination of genome-wide chromatin modifications in primary Wilms tumors, fetal and mature kidney.

2010-05-05 | E-GEOD-20512 | biostudies-arrayexpress

Lin28 sustains early renal progenitors and induces Wilms tumor

Project description:Wilms Tumor, the most common pediatric kidney cancer, evolves from the failure of terminal differentiation of the embryonic kidney. Here we show that over-expression of the heterochronic regulator Lin28 during kidney development in mice markedly expands nephrogenic progenitors by blocking their final wave of differentiation, ultimately resulting in pathology highly reminiscent of Wilms tumor. Gene expression analysis was performed on a total of 8 kidneys samples, including 4 tumors samples from Lin28 transgenic mice and 4 control kidneys

2014-06-01 | E-GEOD-56323 | biostudies-arrayexpress

Lin28 sustains early renal progenitors and induces Wilms tumor

2014-06-01 | GSE56323 | GEO

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

Gene expression profiling of Wilms tumors

Project description:The global gene expression pattern of Wilms tumors in comparison with clear cell sarcoma of the kidney (CCSK) and non-neoplastic fetal and adult kidneys.

2016-02-04 | GSE73209 | GEO

The developmental programme for genesis of the entire kidney is recapitulated in Wilms tumour

Project description:Expression profiling of Wilms tumour samples, which identified molecular signatures of the ureteric bud and collecting duct as well as those of the proximal and distal tubules in triphasic histology tumours. These observations indicate Wilms tumours can arise from a precursor cell capable of generating the entire kidney, such as the cells of the intermediate mesoderm from which both the metanephric mesenchym and ureteric bud are derived.

2017-12-31 | E-MTAB-3516 | biostudies-arrayexpress

Gene expression data from Wilms tumor samples

Project description:Wilms tumor (nephroblastoma) is a pediatric kidney tumor that arises from renal progenitor cells. Since the blastemal type is associated with adverse prognosis, we characterized such Wilms tumors by exome and transcriptome analysis. We detected novel, recurrent somatic mutations affecting the SIX1/2 – SALL1 pathway implicated in kidney development, the DROSHA/DGCR8 microprocessor genes as well as alterations in MYCN and TP53, the latter being strongly associated with dismal outcome. The DROSHA mutations impair the RNase III domains, while DGCR8 exhibits stereotypic E518K mutations in the RNA binding domain - both may skew miRNA representation. SIX1 and SIX2 mutations affect a single hotspot (Q177R) in the homeodomain indicative of a dominant effect. In larger cohorts, these mutations cluster in blastemal and chemotherapy-induced regressive tumors that likely derive from blastemal cells and these are characterized by generally higher SIX1/2 expression. These findings broaden the spectrum of human cancer genes and may open new avenues for stratification and therapeutic leads for Wilms tumors. 53 Wilms tumor samples were selected for RNA extraction and hybridization on Affymetrix Affymetrix Human Genome U133 Plus 2.0 Arrays.

2015-02-18 | E-GEOD-53224 | biostudies-arrayexpress

Gene expression data from Wilms tumor samples

2015-02-18 | GSE53224 | GEO

Somatic mutations in DROSHA and DICER1 impair microRNA biogenesis in Wilms tumors

Project description:Through whole-exome sequencing we identified somatic missense mutations in DICER1 and DROSHA in Wilms tumor, a childhood kidney cancer. DICER1 and DROSHA are key enzymes in the microRNA biogenesis pathway. To determine the effect of these mutations on microRNA expression, we prepared small RNAs from Wilms tumors and used next-generation sequencing to determine the expression levels of microRNAs in the tumors.

2015-04-21 | GSE56955 | GEO

Microarray analaysis of adult and childhood renal tumors.

Project description:Analysis of adult and childhood tumors reveals activation of an E2F3 signature unique to Wilms tumors. Keywords: Disease state analysis Clear cell, chromophobe, papillary (types 1 and 2), oncocytoma, and Wilms tumor were compared to normal kidney tissue. No technical replicates.

2008-06-05 | E-GEOD-11024 | biostudies-arrayexpress

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