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accession-icon GSE11121
The humoral immune system has a key prognostic impact in node-negative breast cancer
  • organism-icon Homo sapiens
  • sample-icon 200 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Estrogen receptor (ER) expression and proliferative activity are established prognostic factors in breast cancer. In a search for additional prognostic motives we analyzed the gene expression patterns of 200 tumors of patients who were not treated by systemic therapy after surgery using a discovery approach. After performing hierarchical cluster analysis, we identified co-regulated genes related to the biological process of proliferation, steroid hormone receptor expression, as well as B cell and T cell infiltration. We calculated metagenes as surrogate for all genes contained within a particular cluster and visualized the relative expression in relation to time to metastasis with principal component analysis. Distinct patterns led to the hypothesis of a prognostic role of the immune system in tumors with high expression of proliferation associated genes. In multivariate Cox regression analysis the proliferation metagene showed a significant association with metastasis-free survival of the whole discovery cohort (Hazard Ratio (HR) 2.20, 95% confidence interval (CI) 1.40-3.46). The B cell metagene showed additional independent prognostic information in carcinomas with high proliferative activity (HR 0.66, 95% CI 0.46 - 0.97). A prognostic influence of the B-cell metagene was independently confirmed by multivariate analysis in a first validation cohort enriched for high grade tumors (n=286, HR 0.78, 95% CI 0.62-0.98), and a second validation cohort enriched for younger patients (n=302, HR 0.83, 95% CI 0.7-0.97). Thus, we could demonstrate in three cohorts of untreated node-negative breast cancer patients, that the humoral immune system plays a pivotal role for metastasis-free survival of carcinomas of the breast.

Publication Title

The humoral immune system has a key prognostic impact in node-negative breast cancer.

Sample Metadata Fields

Disease stage

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accession-icon SRP073183
Analysis of Post-TBI Gene Expression Signature Reveals Tubulins, NFE2L2, NFkB, CD44, and S100A4 as Treatment Targets for Traumatic Brain Injury
  • organism-icon Rattus norvegicus
  • sample-icon 30 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Illumina Genome Analyzer IIx

Description

TBI was induced with lateral fluid-percussion injury in adult male rats. Genome-wide RNA-seq of the perilesional cortex, ipsilateral thalamus and dorsal hippocampus was performed at 3 months post-TBI. The data highlighted chronic transcriptional changes, particularly, in the perilesional cortex and thalamus. Genes showing a significantly altered expression both in the cortex and thalamus were submitted to the LINCS web query to identify novel pharmacotherapies to improve post-TBI outcome. Overall design: TBI was induced to 5 rats, 5 sham operated served as a controls.

Publication Title

Analysis of Post-Traumatic Brain Injury Gene Expression Signature Reveals Tubulins, Nfe2l2, Nfkb, Cd44, and S100a4 as Treatment Targets.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE86615
The dentate gyrus after traumatic brain injury
  • organism-icon Rattus norvegicus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.1 ST Array (ragene11st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Chronically dysregulated NOTCH1 interactome in the dentate gyrus after traumatic brain injury.

Sample Metadata Fields

Sex, Specimen part, Treatment, Time

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accession-icon SRP066667
Etiology matters - Comparing Genomic DNA Methylation Patterns in Three Rat Models of Acquired Epilepsy (Amygdala stimulation – mRNA-seq)
  • organism-icon Rattus norvegicus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Explore DNA methylation in focal amygdala stimulation model of epilepsy and its relationship to gene expression. Overall design: Examination of expression changes in stimulated rats compared to sham operated animals in focal amygdala stimulation model of epilpesy.

Publication Title

Etiology matters - Genomic DNA Methylation Patterns in Three Rat Models of Acquired Epilepsy.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP093386
RNA-seq analysis of ESR1 mutations in T47D and MCF7 cell lines
  • organism-icon Homo sapiens
  • sample-icon 48 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: Transcriptome analysis of ESR1 mutant cells was performed via sequencing total RNA in T47D and MCF7 cell lines containing Y537S and D538G mutations. Overall design: Methods: Individual ESR1 WT and mutant T47D and MCF7 clones were hormone deprived in CSS for three days, pooled, and plated in quadruplicates in 6-well plates. The cells were treated with veh or 1nM E2 for 24 hrs, RNA was isolated and subjected to sequencing. Differential expression analysis was performed by DEseq2 and R was used to conduct statistical analysis tests

Publication Title

Mutation site and context dependent effects of ESR1 mutation in genome-edited breast cancer cell models.

Sample Metadata Fields

Treatment, Subject

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accession-icon GSE50936
SOCS2 expression correlates with tumor malignancy, exerts growth promoting effects and is enhanced by androgens in prostate cancer
  • organism-icon Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Deregulation of cytokine- and growth factor signaling due to altered expression of endogenous regulators is well recognized in prostate and other cancers. Suppressor of cytokine signaling 2 (SOCS2) is a key regulator of growth hormone, IGF and prolactin signaling, that have been implicated in carcinogenesis. In this study we elucidate expression pattern and functional significance of SOCS2 in prostate cancer (PCa). Protein expression analysis employing tissue microarrays from two independent patient cohorts revealed significantly enhanced expression in tumor compared to benign tissue as well as association with Gleason score and disease progression. In vitro and in vivo assays uncovered the involvement of SOCS2 in the regulation of cell growth and apoptosis. Functionally, SOCS2 knockdown inhibited prostate cancer cell proliferation and xenograft growth in a CAM assay. Decreased cell growth after SOCS2 downregulation was associated with cell-cycle arrest and apoptosis. In addition, we prove for the first time that SOCS2 expression is significantly elevated upon androgenic stimulation in androgen receptor-positive cell lines, providing a possible mechanistic explanation for high SOCS2 levels in PCa tissue. Consequently, SOCS2 expression correlated with androgen receptor expression in malignant tissue of patients. Taken together, our study linked increased SOCS2 expression in PCa with a pro-proliferative role in vitro and in vivo.

Publication Title

SOCS2 correlates with malignancy and exerts growth-promoting effects in prostate cancer.

Sample Metadata Fields

Treatment, Time

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accession-icon GSE17483
Stat5-regulated gene expression in human prostate cancer cells
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Transcription factor Stat5 is constitutively active in human prostate cancer but not in normal prostate epithelium. Stat5 activation is associated with prostate cancer lesions of high histological grades, and is present in the majority of castration-resistant recurrent human prostate cancers. The molecular mechnisms underlying constitutive activation of Stat5 in primary and recurrent human prostate cancer are currently unclear.

Publication Title

Stat5 promotes metastatic behavior of human prostate cancer cells in vitro and in vivo.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE24514
Expression data from human MSI colorectal cancer and normal colonic mucosa
  • organism-icon Homo sapiens
  • sample-icon 49 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Microsatellite instability (MSI), caused by defective mismatch repair, is observed in a subset of colorectal cancers (CRCs). We evaluated somatic mutations in microsatellite repeats of genes chosen based on reduced expression in MSI CRC and existence of a coding mononucleotide repeat.

Publication Title

Candidate driver genes in microsatellite-unstable colorectal cancer.

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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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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