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accession-icon GSE39022
Expression data from spleen and lymph node conventional CD11c+ Dendritic cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Spleen and lymph node dendritic cells have a differential capacity do induce and retain iTreg cells. Therefore we performed a comparative analysis of the dendritic cells derived from these two compartments to identify the responsible genes

Publication Title

Migratory, and not lymphoid-resident, dendritic cells maintain peripheral self-tolerance and prevent autoimmunity via induction of iTreg cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE81602
A long noncoding RNA regulates sister chromatid cohesion
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A Long Noncoding RNA Regulates Sister Chromatid Cohesion.

Sample Metadata Fields

Cell line

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accession-icon GSE81599
A long noncoding RNA regulates sister chromatid cohesion [microarray]
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20), Illumina HiSeq 2000

Description

Long noncoding RNAs (lncRNAs) have appeared to be involved in the most diverse cellular processes through multiple mechanisms. Here we describe a previously uncharacterized human lncRNA, CONCR (cohesion regulator noncoding RNA), transcriptionally activated by MYC, which is upregulated in multiple cancer types. The expression of CONCR is cell cycle-regulated, and it is required for cell cycle progression and DNA replication. Moreover, cells depleted of CONCR show severe defects in sister chromatid cohesion, suggesting an essential role for CONCR in cohesion establishment during cell division. CONCR interacts with and regulates the activity of DDX11, a DNA-dependent ATPase and helicase involved in DNA replication. These findings suggest a novel mechanism of action for CONCR in the modulation of DDX11 enzymatic activity, unveiling the direct involvement of a lncRNA in the establishment of sister chromatid cohesion.

Publication Title

A Long Noncoding RNA Regulates Sister Chromatid Cohesion.

Sample Metadata Fields

Cell line

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accession-icon GSE14286
Expression data for biophenotypic leukemia patients treated in St. Jude Children's Research Hospital
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Mixed-lineage leukemias represent about 3-5% of acute leukemias occurring in patients of all ages and comprise several different subtypes (biphenotypic, bilineal, and lineage switch). The optimal therapeutic approach to these cases, especially in pediatric patients, has not been defined. We used microarrays to detail the gene expression of pediatric patients with biophenotypic leukemia.

Publication Title

Acute mixed lineage leukemia in children: the experience of St Jude Children's Research Hospital.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE8879
Gene expression profiling of atypical T-ALL
  • organism-icon Homo sapiens
  • sample-icon 55 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Despite improved therapy, approximately one-fifth of children with acute T-lymphoblastic leukemia (T-ALL) succumb to the disease, suggesting unrecognized biologic heterogeneity that may contribute to drug resistance. We studied leukemic cells, collected at diagnosis, to identify features that could define this high-risk subgroup. A total of 139 patients with T-ALL were treated consecutively from 1992 to 2006 at this institution. Their leukemic cells were examined with multiparameter flow cytometry, single nucleotide polymorphism arrays and other methods of genomic analysis. Survival rates and probabilities of treatment failure were calculated for subgroups considered to have biologically distinct forms of T-ALL.

Publication Title

Early T-cell precursor leukaemia: a subtype of very high-risk acute lymphoblastic leukaemia.

Sample Metadata Fields

Specimen part

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accession-icon GSE17195
Germline genomic variations associated with childhood acute lymphoblastic leukemia
  • organism-icon Homo sapiens
  • sample-icon 44 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

We identified germline single nucleotide polymorphisms (SNPs) associated with childhood acute lymphoblastic leukemia (ALL) and its subtypes. Using the Affymetrix 500K Mapping array and publicly available genotypes, we identified 18 SNPs whose allele frequency differed (P<1x10-5) between a pediatric ALL population (n=317) and non-ALL controls (n=17,958). Six of these SNPs differed (P0.05) in allele frequency among four ALL subtypes. Two SNPs in ARID5B not only differed between ALL and non-ALL groups (rs10821936, P=1.4x10-15, odds ratio[OR]=1.91; rs10994982, P=5.7x10-9, OR=1.62) but also distinguished B-hyperdiploid ALL from other subtypes (rs10821936, P=1.62 x10-5, OR=2.17; rs10994982, P=0.003, OR 1.72). These ARID5B SNPs also distinguished B-hyperdiploid ALL from other subtypes in an independent validation cohort (n=124 children with ALL) (P=0.003 and P=0.0008, OR 2.45 and 2.86, respectively) and were associated with methotrexate accumulation and gene expression pattern in leukemic lymphoblasts. We conclude that germline genomic variations affect susceptibility to and characteristics of specific ALL subtypes.

Publication Title

Germline genomic variants associated with childhood acute lymphoblastic leukemia.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE98928
The human lncRNA LINC-PINT inhibits tumor cell migration through a highly conserved sequence element
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

It is now obvious that the majority of cellular transcripts do not code for proteins, and a significant subset of them are long noncoding RNAs (lncRNAs). Many lncRNAs show aberrant expression in cancer, and some of them have been linked to cellular transformation. However, the underlying mechanisms remain poorly understood. Here we characterize the function of the p53-regulated human lncRNA LINC-PINT in cancer. We found that LINC-PINT acts as tumor suppressor lncRNA. Its expression is downregulated in multiple types of cancer and correlates with good prognosis in lung adenocarcinoma. LINC-PINT inhibits the migration capacity and invasive phenotype of cancer cells in vitro and in vivo, and it does so by repressing a proinvasion gene signature in a PRC2-dependent manner. By applying cross-species conservation analysis combined with functional experimental validations we found that the function of LINC-PINT is highly dependent on a short sequence conserved across mammals, sequence that mediates the interaction with PRC2. We propose that LINC-PINT may function as a molecular exchanger that provides PRC2 to active gene promoters for their silencing, mechanisms that could be shared by other PRC2-interacting lncRNAs.

Publication Title

The human lncRNA LINC-PINT inhibits tumor cell invasion through a highly conserved sequence element.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE25724
Expression data from type 2 diabetic and non-diabetic isolated human islets
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

We performed microarray analysis to evaluate differences in the transcriptome of type 2 diabetic human islets compared to non-diabetic islet samples.

Publication Title

Class II phosphoinositide 3-kinase regulates exocytosis of insulin granules in pancreatic beta cells.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage

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accession-icon SRP011378
DNMT3B7, an aberrant DNMT3B isoform, suppresses growth, induces differentiation, and alters DNA methylation in human neuroblastoma
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

In adult cancers, epigenetic changes and aberrant splicing of the DNMT3B is commonly observed, and the pattern of gene methylation and expression has been shown to be modified by DNMT3B7, a truncated protein of DNMT3B. Much less is known about the mechanism of epigenetic changes in the pediatric cancer neuroblastoma. To investigate if aberrant DNMT3B transcripts alter DNA methylation, gene expression and tumor phenotype in neuroblastoma, we measured DNMT3B isoform expression in primary tumors and cell lines. Higher levels of DNMT3B7 were detected in differentiated ganglioneuroblastomas compared to undifferentiated neuroblastomas, suggesting that expression of DNMT3B7 may induce a less clinically aggressive tumor phenotype. To test this hypothesis, we investigated the effects of forced DNMT3B7 in neuroblastoma cells. We found that DNMT3B7 expression significantly inhibited neuroblastoma cell proliferation in vitro, and in neuroblastoma xenografts, DNMT3B7 decreased angiogenesis and tumor growth. DNMT3B7-positive cells had higher levels of total genomic methylation, and RNA-sequencing revealed a dramatic decrease in expression of FOS and JUN family members, AP1 complex components. Consistent with the established antagonistic relationship between AP1 expression and retinoic acid receptor activity, decreased proliferation and increased differentiation was seen in the DNMT3B7-expressing neuroblastoma cells following treatment with all trans retinoic acid (ATRA) compared to controls. Our results demonstrate that high levels of DNMT3B7 modify the epigenome in neuroblastoma cells, induce changes in gene expression, inhibit tumor growth, and increase sensitivity to ATRA. Further knowledge regarding mechanisms by which DNMT3B7 regulates gene methylation may ultimately lead to the development of therapeutic strategies that reverse the epigenetic aberrations that drive neuroblastoma pathogenesis. Overall design: DNMT3B7, a truncated DNMT3B isoform, was stably transfected into an N-type neuroblastoma cell line (LA1-55n) using a Tet-off inducible system. DNMT3B7 expressing cells were compared to vector control cells after 21 days of induction.

Publication Title

Truncated DNMT3B isoform DNMT3B7 suppresses growth, induces differentiation, and alters DNA methylation in human neuroblastoma.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE14471
Affymetrix U133A array data for 111 pediatric acute myeloid leukemia (AML) samples at diagnosis
  • organism-icon Homo sapiens
  • sample-icon 110 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Genome-wide profiling of Copy Number Alterations (CNA) and Loss of Heterozygosity (LOH), gene expression and resequencing of pediatric AML

Publication Title

Genomic analysis reveals few genetic alterations in pediatric acute myeloid leukemia.

Sample Metadata Fields

Specimen part

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Developed by the Childhood Cancer Data Lab

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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