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accession-icon GSE17548
Expression data from cirrhosis and HCC tissue samples
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Hepatocellular carcinoma (HCC) is the fifth most-common cancer worldwide causing nearly 600,000 deaths esch year. Approximately 80% of HCC develops on the background of cirrhosis.It is necessary to identify novel genes involved in HCC to implement new diagnostic and treatment options. However, the molecular pathogenesis of HCC largely remains unsolved. Only a few genetic alterations, namely those affecting p53, -catenin and p16INK4a have been implicated at moderate frequencies of these cancers. Early detection of HCC with appropriate treatment can decrease tumor-related deaths

Publication Title

Genome-wide transcriptional reorganization associated with senescence-to-immortality switch during human hepatocellular carcinogenesis.

Sample Metadata Fields

Specimen part

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accession-icon GSE17546
Expression data from immortal and senescence-programmed Huh7 clones
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Cellular senescence is a tumor suppressor mechanism, and immortalization facilitates neoplastic transformation. Both mechanisms may be highly relevant to hepatocellular carcinoma (HCC) development and its molecular heterogeneity. Cellular senescence appears to play a major role in liver diseases. Chronic liver diseases are associated with progressive telomere shortening leading senescence that is observed highly in cirrhosis, but also in some HCC. We previously described the generation of immortal and senescence-programmed clones from HCC-derived Huh7 cell line.

Publication Title

Genome-wide transcriptional reorganization associated with senescence-to-immortality switch during human hepatocellular carcinogenesis.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE88721
miRNA and gene expression data from meningioma samples and healthy meningial cell line
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Simultaneous analysis of miRNA-mRNA in human meningiomas by integrating transcriptome: A relationship between PTX3 and miR-29c.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE88720
Gene expression data from meningioma samples and healthy meningial cell line
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

Although meningioma is a common disease, there is a lack of understanding of the underlying molecular mechanisms behind its initiation and progression. We used combined miRNA-mRNA transcriptome analysis to discover novel genes and networks in meningiomas.

Publication Title

Simultaneous analysis of miRNA-mRNA in human meningiomas by integrating transcriptome: A relationship between PTX3 and miR-29c.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE49156
Identification of SDPR as a metastasis suppressor gene
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To identify metastasis suppressor genes, which are functionally compromised in late-stage breast cancer, we compared the gene expression profiles of an established breast cancer progression cell line model and leveraged large amounts of publically available data by applying multiple bioinformatics filters. Here we report the identification of serum deprivation response (SDPR, also known as cavin-2) as a bona fide metastasis suppressor, capable of impairing the metastatic growth of cancer cells while having no effect on the growth of primary tumors.

Publication Title

SDPR functions as a metastasis suppressor in breast cancer by promoting apoptosis.

Sample Metadata Fields

Disease, Disease stage, Cell line

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accession-icon GSE57677
Targeting IL13Ralpha2 activates STAT6-TP63 pathway to suppress breast cancer lung metastasis
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

IL13R2 overexpression promotes metastasis of basal-like breast cancers

Publication Title

Targeting IL13Ralpha2 activates STAT6-TP63 pathway to suppress breast cancer lung metastasis.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon SRP078332
H3.3 depletion has a mild effect on the global transcriptome
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Transcriptomic analysis of H3.3 KO/Kd mouse embryonic fibroblasts (MEFs) Overall design: We isolated total RNA from control shRNA treated or shH3.3A treated H3.3B KO MEFs and carried out Ribozero RNA-seq analysis. RNA-seq analysis was carried out on pooled datasets from biological duplicate experiments.

Publication Title

Histone H3.3 regulates mitotic progression in mouse embryonic fibroblasts.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE66948
Tumor Cell-Derived Periostin Regulates Cytokines That Maintain Breast Cancer Stem Cells
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Basal-like breast cancer (BLBC) cells share phenotypic similarities with cancer stem cells (CSCs) but the underlying molecular basis for this connection remains elusive. We hypothesized that BLBC cells are able to establish a niche permissive to the maintenance of CSCs and found that tumor cell-derived periostin (POSTN), a component of the extracellular matrix, as well as a corresponding cognate receptor, integrin v3, are highly expressed in a subset of BLBC cell lines as well as in cancer stem cell-enriched populations. Furthermore, we demonstrated that an intact periostin-integrin 3 signaling axis is required for the maintenance of breast CSCs. POSTN activates the ERK signaling pathway and regulates NF-B-mediated transcription of key cytokines, namely IL6 and IL8, which in turn mediate downstream activation of STAT3. In summary, these findings suggest that BLBC cells have an innate ability to establish a microenvironmental niche supportive of CSCs.

Publication Title

Tumor Cell-Derived Periostin Regulates Cytokines That Maintain Breast Cancer Stem Cells.

Sample Metadata Fields

Cell line

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accession-icon GSE56736
Genome wide expession analysis of mouse bone marrow derive macrophage (Bmdm) cell stimulated with cytokine and infected with mycobacterium tuberculosis
  • organism-icon Mus musculus
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Bmdm cells were differentiated for 10 days and harvested and culture in six well plate followed by cytokine stimulation after 24 hrs cells were infected with mycobacterium tuberculosis to identify the host factors involved in infection.

Publication Title

IL-4Rα-dependent alternative activation of macrophages is not decisive for Mycobacterium tuberculosis pathology and bacterial burden in mice.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE18070
Smad signaling is required for maintenance of epigenetic gene silencing during breast cancer progression
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In this study, we took advantage of a previously established breast cancer progression cell line model system, which consists of a parental MCF10A (MI) spontaneously immortalized mammary epithelial cell line and two of its derivatives: 1) MCF10ATk.cl2 (MII), a MCF10A H-Ras transformed cell line and 3) MCF10CA1h (MIII), derived from a xenograft of the MII cells in nude mice that progressed to carcinoma (1, 2). These cell lines were previously reported to exhibit distinct tumorigenic properties when re-implanted in nude mice; MI is non-tumorigenic, MII forms benign hyperplastic lesions and MIII forms low-grade, well differentiated carcinomas (2, 3). The advantage of this system is that these cell lines were derived from a common genetic background (MCF10A) and accumulated distinct genetic/epigenetic alterations in vivo enabling them to acquire a range of non-tumorigenic to carcinogenic properties. Our initial studies showed that MIII cells, but not MI or MII, exhibit an EMT phenotype, promoter DNA hypermethylation of epithelial genes and highly invasive properties in vitro.

Publication Title

Smad signaling is required to maintain epigenetic silencing during breast cancer progression.

Sample Metadata Fields

Cell line

View Samples

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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