The expression profiles of 64 neuroblastic tumors (mainly neuroblastoma) were determined on Affymetrix chips HG U133 Plus 2.0.
Somatic and germline activating mutations of the ALK kinase receptor in neuroblastoma.
No sample metadata fields
View SamplesWe sequenced mRNA from transverse slices of embryos from a variety of D. melanogaster mutants (bicoid over-expression, bicoid knockdown, hunchback knocdown, and zelda mutant) at the blastoderm stage to determine genome-wide patterns of gene expression. Overall design: mRNA from transverse sections of single D. melanogaster embryos mutant for patterning TFs was sequenced.
Genome-wide measurement of spatial expression in patterning mutants of <i>Drosophila melanogaster</i>.
Specimen part, Subject
View SamplesWe sequenced mRNA from transverse slices of embryos at the blastoderm stage to determine genome-wide patterns of gene expression. Overall design: mRNA from transverse sections of single D. melanogaster embryos was sequenced
Sequencing mRNA from cryo-sliced Drosophila embryos to determine genome-wide spatial patterns of gene expression.
Specimen part, Disease, Cell line, Subject
View SamplesWe sequenced mRNA according to several library prep protocols with known mixtures of two species of Drosophila in order to establish linear response in each protocol. Overall design: For each library prep protocol, mixtures with 0%, 5%, 10%, and 20% D. virilis total RNA was prepared, then libraries prepared according to instructions.
Low-cost, low-input RNA-seq protocols perform nearly as well as high-input protocols.
Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A stemness-related ZEB1-MSRB3 axis governs cellular pliancy and breast cancer genome stability.
Specimen part, Cell line
View SamplesAberrant cell proliferation, a hallmark of most cancers, requires the escape from intrinsic antitumour barriers. Primary among these is the DNA damage response (DDR). In both cell culture-models and in early stages of tumorigenesis in vivo, activated oncogenes induce DNA replication stress and DNA double-strand breaks (DSBs), leading to DDR activation and p53-dependent apoptosis and/or senescence. The means by which tumour-initiating cells, also termed cancer stem cells (CSCs), circumvent this oncosuppressive response is unknown. Here we demonstrate that the ZEB1 transcription factor provides breast CSCs with the ability to withstand an aberrant mitogenic activity. Its forced expression in human mammary epithelial cells is sufficient to alleviate DNA replicative stress and to decrease the production of reactive oxygen species, an important contributor to DDR and oncogene-induced senescence. Consistently, human breast cancer cells with endogenous ZEB1 expression show two characteristic features: low levels of DSBs and DDR markers, reflecting mitigation of the DNA replication stress, and a low p53 mutation frequency, reflecting a weak selective pressure for inactivation. Using high-throughput sequencing analysis of controlled cellular models, we further demonstrate that ZEB1 delays the onset of structural chromosomal instability (CIN), a known consequence of replicative stress and prevents the emergence of chromosome 8p deletions and 8q amplifications, two prevalent abnormalities in high-grade breast cancers. Supporting these findings, ZEB1 expression discriminates human breast tumours by their copy number alterations (CNAs) and chromosome 8 aberrations. We propose that the tumorigenic potential of CSCs relies upon their unique capacity to tolerate oncogenic stimuli through the alleviation of DNA replication stress.
A stemness-related ZEB1-MSRB3 axis governs cellular pliancy and breast cancer genome stability.
Specimen part
View SamplesTo study role of Lin28/let-7 axis on nephrogenesis, we profiled kidney transcriptom of LIN28 OE, let-7 KO, and their wild-type littermate control mice. Overall design: RNA-seq on kidneys from LIN28B OE, let-7 KO, and their wild-type littermate controls at P3.
Lin28 and let-7 regulate the timing of cessation of murine nephrogenesis.
Cell line, Subject
View SamplesThe long term objective is to create an encyclopedia of the expression levels of all genes in multiple components of the developing kidney. The central thesis is straightforward. The combination of laser capture microdissection (LCM) plus microarray analysis offers a powerful, efficient and effective method for the creation of a global gene expression atlas of the developing kidney. Microarrays with essentially complete genome coverage can be used to quantitate expression levels of every gene in laser capture microdissected components of the developing kidney. The ensuing rapid read-out provides an expression atlas that is more sensitive, more economical and more complete than would be possible by in situ hybridizations alone.
Analysis of early nephron patterning reveals a role for distal RV proliferation in fusion to the ureteric tip via a cap mesenchyme-derived connecting segment.
Sex
View SamplesOur laboratory's interest is in understanding the molecular principles that underlie the regional organization of the mammalian metanephric kidney. Our goal is to generate a detailed spatial map of the cellular expression of selected regulatory genes during mammalian kidney development. The goal of this study is to identify a population of genes that are enriched in the renal vesicle (RV) and its derivatives using Wnt4 mutants.
Analysis of early nephron patterning reveals a role for distal RV proliferation in fusion to the ureteric tip via a cap mesenchyme-derived connecting segment.
Sex
View Samplesbeta-catenin is an essential mediator of canonical Wnt signaling and a central component of the cadherin-catenin epithelial adhesion complex. Dysregulation of beta-catenin expression has been described in pancreatic neoplasia. Newly published studies have suggested that beta-catenin is critical for normal pancreatic development although these reports reached somewhat different conclusions. In addition, the molecular mechanisms by which loss of beta-catenin affects pancreas development are not well understood. The goals of this study then were; 1] to further investigate the role of beta-catenin in pancreatic development using a conditional knockout approach and 2] to identify possible mechanisms by which loss of beta-catenin disrupts pancreatic development. A Pdx1-cre mouse line was used to delete a floxed beta-catenin allele specifically in the developing pancreas, and embryonic pancreata were studied by immunohistochemistry and microarray analysis.
Wnt/beta-catenin signaling is required for development of the exocrine pancreas.
No sample metadata fields
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