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accession-icon GSE23720
High-resolution comparative genomic hybridization of inflammatory breast cancer and identification of candidate genes
  • organism-icon Homo sapiens
  • sample-icon 197 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Inflammatory breast cancer (IBC) is an aggressive form of BC poorly defined at the molecular level. We compared the molecular portraits of 63 IBC and 134 non-IBC (nIBC) clinical samples. Genomic imbalances of 49 IBCs and 124 nIBCs were determined using high-resolution array-comparative genomic hybridization, and mRNA expression profiles of 197 samples using whole-genome microarrays. Genomic profiles of IBCs were as heterogeneous as those of nIBCs, and globally relatively close. However, IBCs showed more frequent complex patterns and a higher percentage of genes with CNAs per sample. The number of altered regions was similar in both types, although some regions were altered more frequently and/or with higher amplitude in IBCs. Many genes were similarly altered in both types; however, more genes displayed recurrent amplifications in IBCs.

Publication Title

High-resolution comparative genomic hybridization of inflammatory breast cancer and identification of candidate genes.

Sample Metadata Fields

Age

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accession-icon SRP102546
Oncogenic BRAF disrupts thyroid morphogenesis and function via Twist expression
  • organism-icon Danio rerio
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Thyroid cancer is common, yet the sequence of alterations that promote tumor formation are incompletely understood. Here we describe a novel model of thyroid carcinoma in zebrafish that reveals temporal changes due to BRAFV600E. Through the use of real-time in vivo imaging we observe disruption in thyroid follicle structure that occurs early in thyroid development. Combinatorial treatment using BRAF and MEK inhibitors reversed the developmental effects induced by BRAFV600E. Adult zebrafish expressing BRAFV600E in thyrocytes developed invasive carcinoma. We identified a gene expression signature from zebrafish thyroid cancer that is predictive of disease free survival in patients with papillary thyroid cancer. Gene expression studies nominated TWIST2 as a key effector downstream of BRAF. Using CRISPR/Cas9 to genetically inactivate a TWIST2 orthologue, we suppressed the effects of BRAFV600E and restored thyroid morphology and hormone synthesis. These data suggest that expression of TWIST2 plays a role in an early step of BRAFV600E-mediated transformation. Overall design: 3 embryo tg-TOM (tg:TdTomato), 3 embryo tg-BRAFV600E-TOM, 3 adult tg-TOM and 5 adult tg-BRAFV600E-TOM biological replicates were sequenced. Strains with tg:TdTomato express the TdTomato fluorophore under control of the zebrafish thyroglobulin promoter (tg).

Publication Title

Oncogenic BRAF disrupts thyroid morphogenesis and function via twist expression.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP076552
Differential gene expression of zebrafish melanocytes and melanomas [RNA-seq]
  • organism-icon Danio rerio
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

We report the gene expression comparison of zebrafish melanocytes and melanomas. These comparisons were used for integrative genomic studies that identified the BMP factor GDF6 as a new oncogene that is specifically expressed in melanomas. Overall design: Examination of gene expression in two different cell types

Publication Title

Ligand-activated BMP signaling inhibits cell differentiation and death to promote melanoma.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP082569
Selenoprotein H is an essential regulator of redox homeostasis that cooperates with p53 in development and tumorigenesis
  • organism-icon Danio rerio
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Selenium, one of a class of selenocysteine-containing proteins (selenoproteins), is an essential micronutrient known for its cancer prevention properties. Selenoprotein H (SepH) is a recently identified nucleolar oxidoreductase whose function is not well understood. Here we report that seph is an essential gene regulating organ development in zebrafish. Metabolite profiling by targeted LCMS/ MS demonstrated that SepH deficiency impairs redox balance by reducing the levels of ascorbate and methionine, while increasing methionine sulfoxide. Transcriptome analysis revealed that SepH deficiency induces an inflammatory response and activates the p53 pathway. Consequently, loss of seph renders larvae susceptible to oxidative stress and DNA damage. Finally, we demonstrate that seph interacts with p53 deficiency in adulthood to accelerate gastrointestinal tumor development. Overall, our findings establish that seph regulates redox homeostasis and suppresses DNA damage. We hypothesize that SepH deficiency may contribute to the increased cancer risk observed in cohorts with low selenium levels. Overall design: 4 WT zebrafish samples and 4 SepH mutant samples

Publication Title

Selenoprotein H is an essential regulator of redox homeostasis that cooperates with p53 in development and tumorigenesis.

Sample Metadata Fields

Subject

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accession-icon GSE26372
Expression analysis of melanoma harvested after GFP or SETDB1 expression
  • organism-icon Danio rerio, Homo sapiens
  • sample-icon 6 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

The histone methyltransferase SETDB1 is recurrently amplified in melanoma and accelerates its onset.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP080709
Germinal-center development of memory B cells driven by IL-9 from follicular helper T cells
  • organism-icon Mus musculus
  • sample-icon 63 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

A subset of GC B cells that have stopped cycling, upregulated CD38 and downregulated BCL-6 is functionally verified as GC-derived memory B cell precursors (GC-MPs). RNA-seq analyses of the transcriptome were used to probe the developmental trajectory of these cells and their responses to IL-9, a cytokine that is found to drive the memory development from the GC. Overall design: Differential gene expression analyses between GC-MP cells and regular GC B cells in G1 phase (GC-MPP cells); Gene expression profiling of different GC subsets in comparison to memory B cells and plasma cells; acute effects of in vivo IL-9 or anti-IL-9 treatment on GC-MP or GC-MPP cells.

Publication Title

Germinal-center development of memory B cells driven by IL-9 from follicular helper T cells.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon GSE46922
Differences in gene expression and cytokines levels between newly diagnosed and chronic pediatric immune thrombocytopenia (ITP)
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Immune thrombocytopenia (ITP) is an autoimmune disease where platelets are destroyed prematurely. In the majority of children the disease resolves but in some it becomes chronic. To investigate whether the two forms of the disease are similar or separate entities we performed DNA microarray analysis of T-cells from newly diagnosed children and children with chronic ITP. We found complete separation of the expression files between the two forms of the disease. Furthermore, the gene expression of several cytokines differed between the two forms of the disease. This was also reflected in plasma with increased levels of IL-16 and TWEAK and lower levels of IL-4 in newly diagnosed compared with chronic ITP. Thus, our data indicate that the two forms of the disease may be separate entities.

Publication Title

Differences in gene expression and cytokine levels between newly diagnosed and chronic pediatric ITP.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE70433
Gene expression in human or mouse brain with iron loading
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Brain iron accumulation affects myelin-related molecular systems implicated in a rare neurogenetic disease family with neuropsychiatric features.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

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accession-icon GSE70430
Substantia nigra (SN) and basal ganglia (BG) gene expression in neurodegenertion with brain iron accumulation (NBIA) cases vs normal controls
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Differential gene expression is assessed in substantia nigra and basal ganglia of neurodegenertion with brain iron accumulation cases (BIA) compared to matched normal controls (c).

Publication Title

Brain iron accumulation affects myelin-related molecular systems implicated in a rare neurogenetic disease family with neuropsychiatric features.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

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accession-icon GSE76948
Expression data from Chinese renal cell carcinoma cells with FSTL1 knocked down
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Clear cell renal cell carcinoma (ccRCC), the major histotype of cancer derived from kidney, is lack of robust prognostic and/or predictive biomarker and powerful therapeutic target. We previously identified that follistatin-like protein 1 (FSTL1) was significantly down-regulated in ccRCC at the transcription level. In the present study, we characterized, for the first time, that FSTL1 immunostaining was selectively positive in the cytoplasm of distal convoluted tubules. The expression of FSTL1 was significantly lower in ccRCC tissues than in adjacent renal tissues (P<0.001), as measured using immunohistochemistry in 69 patients with paired specimens, and lower in most ccRCC cell lines than in human embryonic kidney cells, as measured by quantitative RT-PCR. Multivariate Cox regression analysis in 89 patients with follow-up data showed that FSTL1 expression in tumors conferred a favorable postoperative prognosis independently, with a hazard ratio of 0.325 (95% confidence interval: 0.118-0.894). FSTL1 knockdown promoted anchorage independent growth, mobility, and invasion of ccRCC cell lines and promoted cell cycle from G0/G1 phases into S phase; while over-expression of FSTL1 significantly attenuated cell migration ability in ACHN cells. FSTL1 knockdown resulted in decreased expression of E-cadherin and increased expression of N-cadherin in ccRCC cell lines significantly, indicating that FSTL1 may attenuate epithelial to mesenchymal transition in ccRCC. Microarray assay indicated that NF-B and HIF-2 pathways were activated following FSTL1 knockdown in ccRCC cells. Our study indicates that FSTL1 serves as a tumor suppressor in ccRCC, up-regulation of FSTL1 in cancer cells may be a candidate target therapy for advanced ccRCC.

Publication Title

Follistatin-like protein 1 plays a tumor suppressor role in clear-cell renal cell carcinoma.

Sample Metadata Fields

Specimen part, Cell line

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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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