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accession-icon GSE72359
p53 amplifies Toll-like receptor 5 response in MCF-7 cells
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Using gene expression profiling we characterize the global effect of p53 on the TLR5-mediated transcription in MCF7 cells. We found that combined activation of p53 and TLR5 pathways synergistically increases expression of over 200 genes, mostly associated with immunity and inflammation. The synergy was observed in several human cancer cells and primary lymphocytes.

Publication Title

p53 amplifies Toll-like receptor 5 response in human primary and cancer cells through interaction with multiple signal transduction pathways.

Sample Metadata Fields

Cell line

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accession-icon SRP062163
Genes expression in case of PEV caused by chromosomal rearrangement
  • organism-icon Drosophila melanogaster
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Heterochromatic position effect variegation (PEV) is the epigenetic disruption of genes expression near the new-formed eu-heterochromatic border. We characterized the inversion In(2)A4, demonstrating cis-acting PEV as well as trans-inactivation of the reporter transgenes on the opposite normal chromosome in combination with the inversion. Euchromatic breakpoint of In(2)A4 inversion was localized at 105 bp region (chr2L:21182214-21182318) of the second exon of the Mcm10 gene, the heterochromatic breakpoint is located at the block of dodecasatellite in 2L pericentromeric heterochromatin. In order to check the effects of heterochromatin on neighbor euchromatic genes and estimate the distance of inactivation spreading, we performed RNA-seq analysis of genes expression in larvae and adults females of genotypes A12/A12 (control) and In(2)A4/In(2)A4. Cis-influence of heterochromatin in the inversion causes not only repression, but also activation of genes, and the effects of heterochromatin are different at different developmental stages. Cis-actions affect only a few genes located near the heterochromatin Overall design: Comparison of genes expression in wild type and demonstrating PEV larvae and adults in two repeats each

Publication Title

Trans-inactivation: Repression in a wrong place.

Sample Metadata Fields

Sex, Subject

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accession-icon GSE61272
Expression data of U2OS ER-HA-E2F1 cells induced by OHT with and without knockdown of NFYB
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

E2F1 induces numerous genes, including transcription factors, upon activation. The transcription factors then further cooperates with E2F1 to regulate the target genes and enhance the transcriptional effect.

Publication Title

E2F1-Mediated Induction of NFYB Attenuates Apoptosis via Joint Regulation of a Pro-Survival Transcriptional Program.

Sample Metadata Fields

Cell line

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accession-icon GSE39136
Expression data from U2OS ER-E2F1 cells after FOXO knockdown and E2F1 activation
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Effect of FOXO knockdown on E2F1-mediated transcription

Publication Title

FOXO transcription factors control E2F1 transcriptional specificity and apoptotic function.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE24717
Using a Stem Cell-Based Signature to Guide Therapeutic Selection in Cancer
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Given the very substantial heterogeneity of most human cancers, it is likely that most cancer therapeutics will be active in only a small fraction of any population of patients. As such, the development of new therapeutics, coupled with methods to match a therapy with the individual patient, will be critical to achieving significant gains in disease outcome. One such opportunity is the use of expression signatures to identify key oncogenic phenotypes that can serve not only as biomarkers but also as a means of identifying therapeutic compounds that might specifically target these phenotypes. Given the potential importance of targeting tumors exhibiting a stem-like phenotype, we have developed an expression signature that reflects common biological aspects of various stem-like characteristics. The Consensus Stemness Ranking (CSR) signature is upregulated in cancer stem cell enriched samples, at advanced tumor stages and is associated with poor prognosis in multiple cancer types. Using two independent computational approaches we utilized the CSR signature to identify clinically useful compounds that could target the CSR phenotype. In vitro assays confirmed selectivity of several predicted compounds including topoisomerase inhibitors and resveratrol towards breast cancer cell lines that exhibit a high-CSR phenotype. Importantly, the CSR signature could predict clinical response of breast cancer patients to a neoadjuvant regimen that included a CSR-specific agent. Collectively, these results suggest therapeutic opportunities to target the CSR phenotype in a relevant cohort of cancer patients.

Publication Title

Using a stem cell-based signature to guide therapeutic selection in cancer.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE24578
Basal gene expression of breast cancer cell lines
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Given the very substantial heterogeneity of most human cancers, it is likely that most cancer therapeutics will be active in only a small fraction of any population of patients. As such, the development of new therapeutics, coupled with methods to match a therapy with the individual patient, will be critical to achieving significant gains in disease outcome. One such opportunity is the use of expression signatures to identify key oncogenic phenotypes that can serve not only as biomarkers but also as a means of identifying therapeutic compounds that might specifically target these phenotypes. Given the potential importance of targeting tumors exhibiting a stem-like phenotype, we have developed an expression signature that reflects common biological aspects of various stem-like characteristics. The Consensus Stemness Ranking (CSR) signature is upregulated in cancer stem cell enriched samples, at advanced tumor stages and is associated with poor prognosis in multiple cancer types. Using two independent computational approaches we utilized the CSR signature to identify clinically useful compounds that could target the CSR phenotype. In vitro assays confirmed selectivity of several predicted compounds including topoisomerase inhibitors and resveratrol towards breast cancer cell lines that exhibit a high-CSR phenotype. Importantly, the CSR signature could predict clinical response of breast cancer patients to a neoadjuvant regimen that included a CSR-specific agent. Collectively, these results suggest therapeutic opportunities to target the CSR phenotype in a relevant cohort of cancer patients.

Publication Title

Using a stem cell-based signature to guide therapeutic selection in cancer.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE24716
Expression data from CD133+ and CD133- glioma cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Given the very substantial heterogeneity of most human cancers, it is likely that most cancer therapeutics will be active in only a small fraction of any population of patients. As such, the development of new therapeutics, coupled with methods to match a therapy with the individual patient, will be critical to achieving significant gains in disease outcome. One such opportunity is the use of expression signatures to identify key oncogenic phenotypes that can serve not only as biomarkers but also as a means of identifying therapeutic compounds that might specifically target these phenotypes. Given the potential importance of targeting tumors exhibiting a stem-like phenotype, we have developed an expression signature that reflects common biological aspects of various stem-like characteristics. The Consensus Stemness Ranking (CSR) signature is upregulated in cancer stem cell enriched samples, at advanced tumor stages and is associated with poor prognosis in multiple cancer types. Using two independent computational approaches we utilized the CSR signature to identify clinically useful compounds that could target the CSR phenotype. In vitro assays confirmed selectivity of several predicted compounds including topoisomerase inhibitors and resveratrol towards breast cancer cell lines that exhibit a high-CSR phenotype. Importantly, the CSR signature could predict clinical response of breast cancer patients to a neoadjuvant regimen that included a CSR-specific agent. Collectively, these results suggest therapeutic opportunities to target the CSR phenotype in a relevant cohort of cancer patients.

Publication Title

Using a stem cell-based signature to guide therapeutic selection in cancer.

Sample Metadata Fields

Specimen part

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accession-icon SRP096357
Expression level is a key determinant of E2F1-mediated cell fate
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Purpose: dose response analysis of E2F1 target genes expression in flow-sorted fractions with increasing amounts of fluorescently labled E2F1 Methods:U2OS pTRIPZ-YFP-ER-E2F1 cells were grown in full serum-containing growth medium and treated with 500 ng/ml doxycycline for 48 hours followed by addition of 90 nM OHT for an additional 20 hours. Cells from different YFP fractions were sorted by flow cytometry. mRNA profiles were generated by deep sequencing using Illumina HiSeq 4000. Results: different target genes have different E2F1 activation thresholds. Numerous proliferation-related target genes are induced already by the lowest E2F1-levels. Intermediate E2F1 levels induce cdk inhibitors, which might be responsible for cell cycle arrest. Finally, although some apoptotic E2F1 targets are induced already by low E2F1 levels, many key apoptotic genes require higher E2F1 levels for induction. Conclusions: induction of different cell fates by increasing E2F1 levels might pertain to differential affinities of the targets. Overall design: Methods:U2OS pTRIPZ-YFP-ER-E2F1 cells were grown in full serum-containing growth medium and treated with 500 ng/ml doxycycline for 48 hours followed by addition of 90 nM OHT for an additional 20 hours. Cells from different YFP fractions were sorted by flow cytometry. mRNA profiles were generated by deep sequencing using Illumina HiSeq 4000.

Publication Title

Expression level is a key determinant of E2F1-mediated cell fate.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE8318
Expression from control subplate neurons with few synapses and cocultured subplate neurons with induced synaptogenesis
  • organism-icon Rattus norvegicus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

The transcriptional events accompanying synaptogenesis are largely unknown, or have been studied in systems in which synapse formation occurs gradually over time. With a system in which synaptogenesis is synchronized and controllable, molecular or biochemical techniques can be used to examine cellular events across cultures on a wide scale, as synapses develop.

Publication Title

Synaptogenesis in purified cortical subplate neurons.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE24986
Response of A549 cells treated with Aspergillus fumigatus
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2), Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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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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