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accession-icon GSE104619
Expression data of synchronised mouse embryonic fibroblasts (MEF) and synchronised primary human fibroblasts (NHDF)
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 86 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st), Affymetrix Mouse Gene 2.0 ST Array (mogene20st), Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Assembly of a Parts List of the Human Mitotic Cell Cycle Machinery.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE104615
Expression data of synchronised mouse embryonic fibroblasts (MEF)
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st), Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

Transcriptional programmes involved in the eukaryotic cell cycle are activated sequentially throughout the process. In particular, the set of genes required for S and G2-M phases are highly conserved and induced one after the other.

Publication Title

Assembly of a Parts List of the Human Mitotic Cell Cycle Machinery.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE60998
Exosome Transfer from Stromal to Breast Cancer Cells Regulates Therapy Resistance Pathways
  • organism-icon Homo sapiens
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Exosome transfer from stromal to breast cancer cells regulates therapy resistance pathways.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE60994
Exosome Transfer from Stromal to Breast Cancer Cells Regulates Therapy Resistance Pathways [set 1]
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Stromal communication with cancer cells can influence treatment response. We show that stromal and breast cancer (BrCa) cells utilize paracrine and juxtacrine signaling to drive chemotherapy and radiation resistance. Upon heterotypic interaction, exosomes are transferred from stromal to BrCa cells. RNA within exosomes, which are largely non-coding transcripts and transposable elements, stimulates the pattern recognition receptor RIG-I to activate STAT1-dependent anti-viral signaling. In parallel, stromal cells also activate NOTCH3 on BrCa cells. The paracrine anti-viral and juxtacrine NOTCH3 pathways converge as STAT1 facilitates transcriptional responses to NOTCH3 and expands therapy resistant tumor-initiating cells. Primary human and/or mouse BrCa analysis support the role of anti-viral/NOTCH3 pathways in NOTCH signaling and stroma-mediated resistance, which is abrogated by combination therapy with gamma secretase inhibitors. Thus, stromal cells orchestrate an intricate cross-talk with BrCa cells by utilizing exosomes to instigate anti-viral signaling. This expands BrCa subpopulations adept at resisting therapy and re-initiating tumor growth.

Publication Title

Exosome transfer from stromal to breast cancer cells regulates therapy resistance pathways.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE60995
Exosome Transfer from Stromal to Breast Cancer Cells Regulates Therapy Resistance Pathways [set 2]
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Stromal communication with cancer cells can influence treatment response. We show that stromal and breast cancer (BrCa) cells utilize paracrine and juxtacrine signaling to drive chemotherapy and radiation resistance. Upon heterotypic interaction, exosomes are transferred from stromal to BrCa cells. RNA within exosomes, which are largely non-coding transcripts and transposable elements, stimulates the pattern recognition receptor RIG-I to activate STAT1-dependent anti-viral signaling. In parallel, stromal cells also activate NOTCH3 on BrCa cells. The paracrine anti-viral and juxtacrine NOTCH3 pathways converge as STAT1 facilitates transcriptional responses to NOTCH3 and expands therapy resistant tumor-initiating cells. Primary human and/or mouse BrCa analysis support the role of anti-viral/NOTCH3 pathways in NOTCH signaling and stroma-mediated resistance, which is abrogated by combination therapy with gamma secretase inhibitors. Thus, stromal cells orchestrate an intricate cross-talk with BrCa cells by utilizing exosomes to instigate anti-viral signaling. This expands BrCa subpopulations adept at resisting therapy and re-initiating tumor growth.

Publication Title

Exosome transfer from stromal to breast cancer cells regulates therapy resistance pathways.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE45461
A global DNA methylation and gene expression analysis of early human B-cell development reveals a demethylation signature and transcription factor network.
  • organism-icon Homo sapiens
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A global DNA methylation and gene expression analysis of early human B-cell development reveals a demethylation signature and transcription factor network.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE45460
Expression data from early human B-cell development
  • organism-icon Homo sapiens
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

A global DNA methylation and gene expression analysis of early human B-cell development reveals a demethylation signature and transcription factor network. Nucleic Acids Res. 2012 Dec;40(22):11339-51.

Publication Title

A global DNA methylation and gene expression analysis of early human B-cell development reveals a demethylation signature and transcription factor network.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP098688
Epigenetic mechanisms underlie the crosstalk between growth factors and a steroid hormone [HCT RNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Growth factors (GFs) suppression by steroid hormones recurs in embryology and is co-opted in pathology. While studying mammary cell migration, which is stimulated by GFs and antagonized by glucocorticoids (GCs), we found that GCs inhibit positive feedback loops activated by GFs and stimulate the reciprocal negative loops. Although no alterations in DNA methylation accompany the transcriptional events instigated by either stimulus, forced demethylation of distal regions broadened the repertoire of inducible genes. Our data indicate that the crosstalk involve transcription factors like p53 and NF-kB, along with reduced pausing (and traveling) of RNA polymerase II (RNAPII) at the promoters (and bodies) of GF-inducible genes. In addition, while GFs hyper-acetylated chromatin at unmethylated promoters and enhancers of genes involved in motility, GCs hypo-acetylated the corresponding regions. In conclusion, stably unmethylated genomic regions that encode feedback regulatory modules and differentially recruit RNAPII and acetylases/deacetylases underlie suppression of growth factor signaling by glucocorticoids. Overall design: RNA-Seq – EGF treatemnt for 60 min of WT and DNMT1a and DNMT3b double-knockout HCT116 cells

Publication Title

Epigenetic mechanisms underlie the crosstalk between growth factors and a steroid hormone.

Sample Metadata Fields

Treatment, Subject

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accession-icon GSE56602
Two-Track Epigenetic Remodeling and Backtracking to Embryonic Stem Cell Bivalency in B-cell Acute Lymphoblastic Leukemias
  • organism-icon Homo sapiens
  • sample-icon 81 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st), Illumina HumanMethylation450 BeadChip (HumanMethylation450_15017482), Illumina HiSeq 2000

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Epigenetic remodeling in B-cell acute lymphoblastic leukemia occurs in two tracks and employs embryonic stem cell-like signatures.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE56599
Expression data of pediatric B-cell acute leukemias
  • organism-icon Homo sapiens
  • sample-icon 81 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We investigated DNA methylomes of 227 pediatric B-cell acute lymphoblastic leukemias (B-ALLs) using whole-genome bisulfite sequencing and high-definition microarrays, along with RNA expression profiles.

Publication Title

Epigenetic remodeling in B-cell acute lymphoblastic leukemia occurs in two tracks and employs embryonic stem cell-like signatures.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
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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)

fund-icon Fund the CCDL

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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