The concept of tumor stem cells (TSCs) provides a new paradigm for understanding tumor biology, although it remains unclear whether TSCs will prove to be a more robust model than traditional cancer cell lines. We demonstrate marked phenotypic and genotypic differences between primary human tumor-derived TSCs and their matched glioma cell lines. TSCs derived directly from primary glioblastomas harbor extensive similarities to normal NSC and recapitulate the genotype, gene expression patterns and in vivo biology of human glioblastomas. By contrast, the matched, traditionally grown tumor cell lines do not secondary to in vitro genomic alterations. These findings suggest that TSCs may be a more reliable model than many commonly utilized cancer cell lines for understanding the biology of primary human tumors. Analysis of gene expression data is described in Lee et al., Cancer Cell, 2006.
Tumor stem cells derived from glioblastomas cultured in bFGF and EGF more closely mirror the phenotype and genotype of primary tumors than do serum-cultured cell lines.
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View SamplesGliomas are mostly incurable secondary to their diffuse infiltrative nature. Thus, specific therapeutic targeting of invasive glioma cells is an attractive concept. As cells exit the tumor mass and infiltrate brain parenchyma, they closely interact with a changing micro-environmental landscape that sustains tumor cell invasion.
Identification of molecular pathways facilitating glioma cell invasion in situ.
Specimen part
View SamplesThe purpose of our study was to explore the relevance of the FGF13 protein in a NSCLC cell line Overall design: RNA seq was performed on H460 cells transiently transfected with siRNA against FGF13 (siFGF13) or control siRNA (siC)
Regulatory module involving FGF13, miR-504, and p53 regulates ribosomal biogenesis and supports cancer cell survival.
Specimen part, Cell line, Subject
View SamplesEmbryonic stem cells (ESCs) maintain high genomic plasticity, essential for their capacity to enter diverse differentiation pathways. Post-transcriptional modifications of chromatin histones play a pivotal role in maintaining this plasticity. We now report that one such modification, monoubiquitylation of histone H2B on lysine 120 (H2BK120ub1), catalyzed by the E3 ligase RNF20, increases during ESC differentiation and is required for efficient execution of this process. This increase is particularly important for the transcriptional induction of long genes during ESC differentiation. Furthermore, we identify USP44 as a deubiquitinase whose downregulation by differentiation signals contributes to the increase in H2BK120ub1. Our findings suggest that optimal ESC differentiation requires dynamic changes in H2B ubiquitylation patterns, which must occur in a timely and well-coordinated manner.
RNF20 and USP44 regulate stem cell differentiation by modulating H2B monoubiquitylation.
Cell line, Treatment
View SamplesThis is Rembrandt gene expression data (Affymetrix HG-U133Plus2).
Rembrandt: helping personalized medicine become a reality through integrative translational research.
Specimen part, Disease, Disease stage
View SamplesTranscriptome analysis of growth hormone dependant genes in glomerular podocytes
Growth hormone (GH)-dependent expression of a natural antisense transcript induces zinc finger E-box-binding homeobox 2 (ZEB2) in the glomerular podocyte: a novel action of gh with implications for the pathogenesis of diabetic nephropathy.
Specimen part, Treatment
View SamplesAnalyses of six Ts1Cje (Down syndrome) and six normal littermate (2N) mouse brains at postnatal day 0.
Dosage-dependent over-expression of genes in the trisomic region of Ts1Cje mouse model for Down syndrome.
No sample metadata fields
View SamplesAnalyses of six Ts1Cje (Down syndrome) and six normal littermate (2N) mouse brains at postnatal day 0.
Dosage-dependent over-expression of genes in the trisomic region of Ts1Cje mouse model for Down syndrome.
No sample metadata fields
View SamplesAnalyses of six Ts1Cje (Down syndrome) and six normal littermate (2N) mouse brains at postnatal day 0.
Dosage-dependent over-expression of genes in the trisomic region of Ts1Cje mouse model for Down syndrome.
No sample metadata fields
View SamplesWe developed a computational framework that integrates chromosomal copy number and gene expression data for detecting aberrations that promote cancer progression. We demonstrate the utility of this framework using a melanoma dataset. Our analysis correctly identified known drivers of melanoma and predicted multiple novel tumor dependencies. Two dependencies, TBC1D16 and RAB27A, confirmed empirically, suggest that abnormal regulation of protein trafficking contributes to proliferation in melanoma. Together, these results demonstrate the ability of integrative Bayesian approaches to identify novel candidate drivers with biological, and possibly therapeutic, importance in cancer.
An integrated approach to uncover drivers of cancer.
Cell line
View Samples