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accession-icon GSE6786
HeLa cells and MCF10A cells subject to EGF stimulation
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A module of negative feedback regulators defines growth factor signaling.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE6783
Expression data from HELA cells subject to EGF stimulation
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

HELA cells derived from human cervical tumor were subjected to EGF stimulation for 0,20,40,60,120,240 and 480 minutes.

Publication Title

A module of negative feedback regulators defines growth factor signaling.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE6784
Expression data from MCF10A cells subject to EGF stimulation
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

MCF10A cells derived from spontaneously immortalized normal human mammary epithel were subjected to EGF/SERUM stimulation for 0,20,40,60,120,240 and 480 minutes.

Publication Title

A module of negative feedback regulators defines growth factor signaling.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE13909
Molecular signature of cell cycle exit induced in human T lymphoblasts by IL-2 withdrawal
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Molecular mechanisms of cell cycle exit are poorly understood. A group of genes required for cell cycle exit and maintenance of cell quiescence in human fibroblasts following serum deprivation has been recently identified. Studies on lymphocytes following growth factor deprivation-induced cell cycle exit have predominantly focused on the initiation of apoptosis. A set of genes involved in lymphocyte quiescence have also been identified among genes highly expressed in resting lymphocytes and down-regulated after cell activation. In our study, proliferating IL-2-dependent human T cells were forced to exit cell cycle by growth factor withdrawal, and their gene expression profiles were examined.

Publication Title

Molecular signature of cell cycle exit induced in human T lymphoblasts by IL-2 withdrawal.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE54269
A Molecular Portrait of the Homologous Recombination DNA Repair via Genome-wide Transcriptome Profiling
  • organism-icon Homo sapiens
  • sample-icon 68 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Genome-wide transcriptome profiling of homologous recombination DNA repair.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE54268
Expression data of ATM, ATR, CHK1, CHK2, and 53BP1 shRNA knockdown and control shRNA in MCF-10A cells
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

Homologous recombination-mediated DNA repair deficiency (HRD) predisposes to cancer development, but also provides therapeutic opportunities. Here, we identified an HRD gene signature that robustly predicted HRD status. Unexpectedly, concurrent loss of PTEN in BRCA1-deficient cells might extensively rewire the HR repair network and confer resistance to PARP inhibitor, partially through over-expression of TTK. We used the HRD gene signature as a drug discovery tool and found several PARP-inhibitor-synergizing agents through the connectivity map. Thus gene expression profiling can be used to define the functional status of the HR repair network providing prognostic and therapeutic information.

Publication Title

Genome-wide transcriptome profiling of homologous recombination DNA repair.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE54267
Expression data of CHK1 shRNA knockdown and control shRNA in U2OS cells
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Homologous recombination-mediated DNA repair deficiency (HRD) predisposes to cancer development, but also provides therapeutic opportunities. Here, we identified an HRD gene signature that robustly predicted HRD status. Unexpectedly, concurrent loss of PTEN in BRCA1-deficient cells might extensively rewire the HR repair network and confer resistance to PARP inhibitor, partially through over-expression of TTK. We used the HRD gene signature as a drug discovery tool and found several PARP-inhibitor-synergizing agents through the connectivity map. Thus gene expression profiling can be used to define the functional status of the HR repair network providing prognostic and therapeutic information.

Publication Title

Genome-wide transcriptome profiling of homologous recombination DNA repair.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE54264
Expression data of Brti1 shRNA knockdown and control shRNA in MCF-10A cells
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

Homologous recombination-mediated DNA repair deficiency (HRD) predisposes to cancer development, but also provides therapeutic opportunities Here, we identified an HRD gene signature that robustly predicted HRD status Unexpectedly, concurrent loss of PTEN in BRCA1-deficient cells might extensively rewire the HR repair network and confer resistance to PARP inhibitor, partially through over-expression of TTK We used the HRD gene signature as a drug discovery tool and found several PARP-inhibitor-synergizing agents through the connectivity map Thus gene expression profiling can be used to define the functional status of the HR repair network providing prognostic and therapeutic information

Publication Title

Genome-wide transcriptome profiling of homologous recombination DNA repair.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon SRP118933
Osteoblasts remotely supply lung tumors with cancer-promoting SiglecFhigh neutrophils
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

RNAseq (3''DGE) profiles of osteoblasts from four lung cancer-bearing mice and three tumor-free mice. Overall design: Osteoblasts were FACS-sorted using the following markers: CD45-CD31-Terr119-GFP+ from lineage depleted bone and bone marrow tissue of lung tumor-bearing or tumor-free age-, sex- and litter-matched KrasLSL-G12D/WT;p53Flox/Flox (KP)-Ocn GFP mice. Total RNA was prepared using the Trizol method followed cDNA preparation, amplification, Illumina adapter ligation and 3''end sequencing by Illumina HiSeq 2500

Publication Title

Osteoblasts remotely supply lung tumors with cancer-promoting SiglecF<sup>high</sup> neutrophils.

Sample Metadata Fields

Sex, Age, Specimen part, Subject

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)

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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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