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MicroRNA-expression profiling according to the Wilms tumor 1 (WT1) single nucleotide polymorphism rs16754 in adult de novo cytogenetically normal acute myeloid leukemia patients 60 years.\//\<

ABSTRACT: microRNA-expression profiling according to the Wilms tumor 1 (WT1) single nucleotide polymorphism rs16754 in adult de novo cytogenetically normal acute myeloid leukemia patients <60 years.

ORGANISM(S): Homo sapiens

SUBMITTER: Guido Marcucci

PROVIDER: E-TABM-1166 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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MicroRNA-expression profiling according to the Wilms tumor 1 (WT1) single nucleotide polymorphism rs16754 in adult de novo cytogenetically normal acute myeloid leukemia patients >=60 years.

Project description:MicroRNA-expression profiling according to the Wilms tumor 1 (WT1) single nucleotide polymorphism rs16754 in adult de novo cytogenetically normal acute myeloid leukemia patients >=60 years.

2012-06-09 | E-TABM-1167 | biostudies-arrayexpress

Gene-expression profiling according to the Wilms tumor 1 (WT1) single nucleotide polymorphism rs16754 in adult de novo cytogenetically normal acute myeloid leukemia.

Project description:Gene-expression profiling according to the Wilms tumor 1 (WT1) single nucleotide polymorphism rs16754 in adult de novo cytogenetically normal acute myeloid leukemia.

2012-06-09 | E-TABM-1165 | biostudies-arrayexpress

Transcription profiling of human WT1-mutant versus WT1 wild-type Wilms tumors

Project description:Gain-of-function mutations in exon 3 of beta-catenin (CTNNB1) are specific for Wilms' tumors that have lost WT1, but 50% of WT1-mutant cases lack such "hot spot" mutations. To ask whether stabilization of beta-catenin might be essential after WT1 loss, and to identify downstream target genes, we compared expression profiles in WT1-mutant versus WT1 wild-type Wilms' tumors. Supervised and nonsupervised hierarchical clustering of the expression data separated these two classes of Wilms' tumor. The WT1-mutant tumors overexpressed genes encoding myogenic and other transcription factors (MOX2, LBX1, SIM2), signaling molecules (TGFB2, FST, BMP2A), extracellular Wnt inhibitors (WIF1, SFRP4), and known beta-catenin/TCF targets (FST, CSPG2, CMYC). Beta-Catenin/TCF target genes were overexpressed in the WT1-mutant tumors even in the absence of CTNNB1 exon 3 mutations, and complete sequencing revealed gain-of-function mutations elsewhere in the CTNNB1 gene in some of these tumors, increasing the overall mutation frequency to 75%. Lastly, we identified and validated a novel direct beta-catenin target gene, GAD1, among the WT1-mutant signature genes. These data highlight two molecular classes of Wilms' tumor, and indicate strong selection for stabilization of beta-catenin in the WT1-mutant class. Beta-Catenin stabilization can initiate tumorigenesis in other systems, and this mechanism is likely critical in tumor formation after loss of WT1. Experiment Overall Design: Identification of WNT/Beta-Catenin or WT1 target genes. 39 individual samples.

2008-06-14 | E-GEOD-6120 | biostudies-arrayexpress

Wilms' tumor 1 WT1(-KTS) isoform time course induction in U2OS cells

Project description:The Wilms' tumor suppressor gene (WT1) encodes a zinc finger transcription factor that plays important roles during development of several organs including metanephric kidneys. A number of WT1 target genes have been identified, but the detailed mechanisms by which WT1 orchestrates renal development remain elusive. To identify WT1 target genes relevant to development, genome-wide expression profiling was performed using oligonucleotide microarrays representing 39,000 human transcripts Keywords: Wilms' tumor 1 (WT1) gene, -KTS isoform; time course

2007-06-21 | GSE5117 | GEO

Oligonucleotide expression microarray data for analysis of Wilms tumor 1 gene (WT1) mutations in cytogenetically normal acute myeloid leukemia (AML) patient samples

Project description:Oligonucleotide expression microarray data used for expression signature associated with WT1 mutations in cytogenetically normal AML patient samples

2011-06-17 | E-TABM-1020 | biostudies-arrayexpress

CTNNB1 mutations and overexpression of Wnt/beta-catenin target genes in WT1-mutant Wilms' tumors

2006-10-28 | GSE6120 | 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

Oviductal fluid LC-MS/MS - The Wilms tumor protein Wt1 contributes to female fertility by regulating oviductal proteostasis

Project description:After fertilization the developing mammalian embryo migrates through the oviduct before it implants in the uterus. In order to prevent tubal pregnancy or failed implantation, development and migration of the embryo has to be tightly coordinated1. The precise molecular basis for the regulation of this maternal-embryonic interaction is largely unknown. Here we show that the Wilms tumor suppressor protein Wt1 is a critical regulator of the interaction between the maternal environment and the early embryo. Our results indicate that subfertility in Wt1ko/+ females is a maternal effect caused by the Wt1-dependent de-regulation of Prss29, encoding a serine protease. Notably, blocking Prss29 activity was sufficient to rescue subfertility in Wt1ko/+ female mice indicating Prss29 as a critical factor in female fertility. Furthermore, we have identified a missense mutation in a patient with idiopathic infertility leading to an amino acid exchange within the zinc finger domain of WT1 and resulting in reduced DNA binding. We demonstrate that Wt1 represses expression of Prss29 and that its de-repression and precocious expression in the oviduct interferes with pre-implantation development. Our study reveals a novel role for Wt1 in early mammalian development and identifies proteases as critical mediators of the maternal-embryonic crosstalk. We believe that our data regarding the importance of a proteostatic environment in the oviduct are also relevant for female fertility in humans. We anticipate that our findings will form the basis for the identification of further causes of idiopathic infertility.

2017-04-04 | PXD003283 | Pride

Classification of a frameshift/extended and a stop mutation in WT1 as gain of function mutations which activate cell cycle genes and promote Wilms tumor cell proliferation

Project description:The Wilms tumor 1 (WT1) gene encodes a zinc finger transcription factor important for normal kidney development. WT1 is a suppressor for Wilms tumor development and an oncogene for diverse malignant tumors. We recently established cell lines from primary Wilms tumors and identified the corresponding WT1 mutations (see GSE18058). To investigate the function of mutant WT1 proteins we performed WT1 knockdown experiments in primary Wilms tumor cell lines with a frameshift/extension (p.V432fsX87 = Wilms3) and a stop mutation (p.P362X = Wilms2) of WT1, followed by genome wide gene expression analysis. A detailed analysis of these gene expression data using MetaCore enabled us to classify the WT1 mutations as gain of function mutations. The mutant WT1Wilms2 and WT1Wilms3 proteins acquired an ability to modulate the expression of a highly significant number of genes from the G2/M phase of the cell cycle, and WT1 knockdown experiments showed that they are required for Wilms tumor cell proliferation. Data from the literature show that p53 negatively regulates the activity of a large number of these genes which are also part of a core proliferation cluster in diverse human cancers. Our data strongly suggest that mutant WT1 proteins facilitate expression of these cell cycle genes by antagonizing transcriptional repression mediated by p53. In light of this it is important to note that mutant WT1 has an ability to physically interact with the tumor suppressor p53. Together the findings show for the first time, that mutant WT1 proteins have a gain of function and act as oncogenes for Wilms tumor development by regulating Wilms tumor cell proliferation.

2014-05-12 | GSE54635 | GEO

A novel unusual chromosome 11 abnormality: a homozygous somatic deletion of the entire WT1 gene within a heterozygous 11p13 deletion and UPD limited to 11p15 in a Wilms tumor and establishment of an immortalized cell line

Project description:We describe a stromal predominant Wilms tumor with a complex, tumor specific chromosome 11 aberration: a homozygous deletion of the entire WT1 gene within a heterozygous 11p13 deletion and an additional region of uniparental disomy (UPD) limited to 11p15.5-p15.2 including the IGF2 gene. The tumor carried a heterozygous p.T41A mutation in CTNNB1. Cells established from the tumor carried the same chromosome 11 aberration, but a different, homozygous p.S45Î CTNNB1 mutation. Uniparental disomy (UPD) 3p21.3pter lead to the homozygous CTNNB1 mutation. The tumor cell line was immortalized with telomerase (TERT) and a novel triple ts mutant SV40 large T antigen (LT). This cell line is cytogenetically stable and can be grown indefinitely. It is a valuable tool to study the effect of a complete lack of WT1 in tumor cells. The tumor cell line and the immortalized cells have a limited potential for muscle/osteogenic/adipogenic differentiation similar to all other WT1 mutant cell lines. Array expression experiment of Wilms tumor cell lines

2016-06-01 | E-GEOD-71265 | biostudies-arrayexpress

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