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accession-icon GSE65505
Gene expression profiling in response to radiation treatment in human breast cancer
  • organism-icon Homo sapiens
  • sample-icon 61 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Treatment-related morbidities have been linked to the large post-operative treatment volumes required for external beam partial breast irradiation (PBI). Alternative PBI techniques require equipment that is not readily available. To address these issues, we designed a phase I trial utilizing widely available technology to 1) evaluate the safety of a single radiation treatment delivered preoperatively to the small-volume, intact breast tumor and 2) identify imaging and genomic markers of radiation response.

Publication Title

FAS Death Receptor: A Breast Cancer Subtype-Specific Radiation Response Biomarker and Potential Therapeutic Target.

Sample Metadata Fields

Specimen part

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accession-icon GSE59732
Gene expression profiling in response to radiation treatment in breast cancer [cell lines]
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Introduction: Breast radiotherapy is currently one size fits all regardless of breast cancer subtype (eg. luminal, basal). However, recent clinical data suggests that radiation response may vary significantly among subtypes. Therefore, current practice leads to over- or under-treatment of women whose tumors are more or less radiation responsive. We hypothesized that this clinical variability may be due, in part, to differences in cellular radiation response. Methods: We exposed 16 biologically-diverse breast tumor cell lines to 0 or 5GY radiation. Microarray analysis was performed on RNA harvested from those cell lines. Samples were run in triplicate. Following quality assessment, differential gene expression analysis was performed using a two-way multiplicative linear mixed-effects model. A candidate radiation response biomarkers with biologically plausible role in radiation response, were identified and confirmed at the RNA and protein level with qPCR and Western blotting assays. Induction in human breast tumors was confirmed in 32 patients with paired pre- and post-radiation tumor samples using IHC and microarray analysis. Quantification of protein was performed in a blinded manner and included positive and negative controls.

Publication Title

FAS Death Receptor: A Breast Cancer Subtype-Specific Radiation Response Biomarker and Potential Therapeutic Target.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon E-MEXP-1074
Transcription profiling by array of excisional biopsy wounds from young and old human subjects to measure the influence of age on cutaneous wound healing
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

The aim of this experiment was measure the influence of age on cutaneous wound healing using human subjects. Increaded age has been associated with delayed wound healing in mouse models and in humans. Gene expression was compared between excisional biopsy wounds from young and old subjects.

Publication Title

Estrogen, not intrinsic aging, is the major regulator of delayed human wound healing in the elderly.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon E-MEXP-1232
Transcription profiling by array of skin wound samples from rats treated with the 5alpha-reductase inhibitor MK-434
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Expression 230A Array (rae230a)

Description

The present study aimed to delineate the central mechanisms by which androgens delay wound repair. Blocking the conversion of testosterone to 5alpha-dihydrotestosterone (DHT) by 5alpha-reductase limits its ability to impair skin wound healing, suggesting that DHT is a more potent inhibitor of repair than is testosterone. This study aims to identify, through transcription profiling, potential mechanisms by which the 5alpha-reductase inhibitor MK-434 modulates repair. Microarray analysis of wound RNA samples from rats in which the transformation of testosterone to DHT is prevented has identified biological processes and key individual genes through which DHT may contribute to the altered healing profile in such animals. These include genes with putative roles in wound contraction and re-epithelialization.

Publication Title

5alpha-dihydrotestosterone (DHT) retards wound closure by inhibiting re-epithelialization.

Sample Metadata Fields

Sex, Age, Specimen part, Compound

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accession-icon E-MEXP-209
Transcription profiling of wounds from ovariectomized MIF null mice and controls to investigate the role of MIF during wound healing using BALB/C MIF null mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

The aim of this experiment was to investigate the role of MIF during wound healing using BALB/C MIF null mice and in the context of reduced estrogen-associated impaired healing using ovariectomized mice (a mouse model of age-associated delayed healing). Ageing is associated with delayed cutaneous wound healing resulting from reduced estrogen levels. Macrophage migration inhibitory factor (MIF - NCBI RefSeq: NM_010798) is thought to mediate the effects of estrogen on wound healing. Gene expression was compared between wounds from ovariectomized MIF null mice and controls.

Publication Title

Macrophage migration inhibitory factor: a central regulator of wound healing.

Sample Metadata Fields

Sex, Age, Specimen part, Subject

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accession-icon GSE11484
Gene expression analysis of ctrl_islets versus VhlhKO_islets
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Understanding the nature of the various glucose-derived signals for insulin secretion (both triggering and amplifying) is essential for gaining insight into the functional failure of the beta-cells in diabetes and the development of drugs for correcting this problem. The beta-cells uniquely couple changes in cellular metabolism to electrical activity and thus insulin release. In mice, beta-cell specific deletion of the von Hippel-Lindau (VHL) tumor suppressor protein leads to the activation of a HIF transcription program that includes genes involved in glycolysis, suppression of mitochondrial activity and lactate production. This reprogramming of cellular metabolism results in abnormal insulin secretion properties.

Publication Title

PVHL is a regulator of glucose metabolism and insulin secretion in pancreatic beta cells.

Sample Metadata Fields

Sex, Age

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accession-icon GSE41058
Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.
  • organism-icon Caenorhabditis elegans
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Genome Array (celegans)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Competition between virus-derived and endogenous small RNAs regulates gene expression in Caenorhabditis elegans.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE41056
Analysis of gene expression changes upon infection of C.elegans with Orsay virus
  • organism-icon Caenorhabditis elegans
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Genome Array (celegans)

Description

Analysis of the transcriptional response to viral infection in C.elegans.

Publication Title

Competition between virus-derived and endogenous small RNAs regulates gene expression in Caenorhabditis elegans.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP015836
Changes in small RNAs upon Viral infection of C.elegans
  • organism-icon Caenorhabditis elegans
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Attempt to identify small non-coding RNAs that change in levels as a result of viral infection of C.elegans Overall design: Small non-coding RNA (18-30nt) was extracted from animals either infected with Orsay virus or uninfected as indicated.

Publication Title

Competition between virus-derived and endogenous small RNAs regulates gene expression in Caenorhabditis elegans.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP016138
GRO-seq of Drosophila embryos at 2-2.5 hours and 3-3.5 hours after egg laying (AEL)
  • organism-icon Drosophila melanogaster
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

The transition in developmental control from maternal to zygotic gene products marks a critical step in early embryogenesis. Here, we use GRO-seq analysis to map the genome-wide RNA polymerase distribution during the Drosophila maternal to zygotic transition. This analysis unambiguously identifies the zygotic transcriptome, and provides insight into its mechanisms of regulation. Overall design: Two replicates of GRO-seq at each time point.

Publication Title

Extensive polymerase pausing during Drosophila axis patterning enables high-level and pliable transcription.

Sample Metadata Fields

Specimen part, Cell line, Subject, Time

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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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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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