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accession-icon GSE25976
Expression profiles of CD24-/CD44+/ESA+ population in MDA-MB-231 and its highly metastatic variants.
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Breast cancer is a curable disease if it is diagnosed at an early stage. However, only little options are left once the tumor is metastasized to distant organs, and more than 90% of breast cancer death is attributed to metastatic disease. The process of metastasis is highly complex and involves many steps for successful colonization of tumor cells at a target organ. According to the cancer stem cell (CSC) theory, which still remains a hypothesis, these metastatic cells must have stem cell-like capability for their self-renewal in addition to their invasive ability. Therefore, it has been predicted that a metastatic stem cell, which is distinct from a cancer stem cell, must exist in the primary tumor mass. To identify genes that are involved in metastasis of CSCs, we isolated CSC populations from a well-established model cell line of breast cancer, MDA-MB231, and that of highly metastatic variants, 231BoM-1833 and 231BrM-2a, using CD24, CD44 and EpCAM (ESA), which have been identified as surface markers for CSCs in breast cancers. Overall yield of CSCs from these cells ranged from 2% to 4%. We then performed global expression profile analysis for these CSCs using the Affymetrix Human Gene 1.0ST array.

Publication Title

Hyaluronan synthase HAS2 promotes tumor progression in bone by stimulating the interaction of breast cancer stem-like cells with macrophages and stromal cells.

Sample Metadata Fields

Cell line

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accession-icon SRP140471
A Zebrafish Acromegaly Model Elevates DNA Damage and Impairs DNA Repair Pathways
  • organism-icon Danio rerio
  • sample-icon 27 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Acromegaly is a pathological condition due to excess growth hormone (GH) secretion. Acromegaly patients exhibit a deterioration of health and many associated complications, such as cardiovascular issues, arthritis, kidney diseases, muscular weakness, and colon cancer. Since these complications are generalized throughout the body, we investigated the effect of GH excess on cellular integrity. Here, we established stable acromegaly model zebrafish lines that overexpress tilapia GH and the red fluorescence protein (RFP) reporter gene for tracking GH gene expression throughout generations, and performed RNA-Seq data analysis from different organs. Intriguingly, heatmap and Expression2Kinases (X2K) analysis revealed the enrichment of DNA damage markers in various organs. Moreover, H2A.X immunostaining analysis in acromegaly zebrafish larvae and the adult acromegaly model brain and muscle showed a robust increase in the number of DNA-damaged cells. Using Gene Set Enrichment Analysis (GSEA), we found that the acromegaly zebrafish model had impaired DNA repair pathways in the liver, such as double-strand break (DSB), homologous recombination repair (HRR), non-homologous end joining (NHEJ), nucleotide excision repair (NER), and translesion synthesis (TLS). Interestingly, the impairment of DNA repair was even more prominent in acromegaly model than in aged zebrafish (three years old). Thus, our study demonstrates that affection of cellular integrity is characteristic of acromegaly Overall design: Total mRNA obtained from 1-years old acromegaly zebrafish model muscle, brain, kidney, liver and 3-day old larvae compared to wild-type (WT) zebrafish were generated by deep sequencing using Illumina.

Publication Title

An Acromegaly Disease Zebrafish Model Reveals Decline in Body Stem Cell Number along with Signs of Premature Aging.

Sample Metadata Fields

Age, Specimen part, Subject

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accession-icon SRP060414
BMP signaling in mouse embryonic stem cells (ESCs) in the naïve and primed pluripotent states [RNA-Seq]
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Carrying out both RNA-seq and Smad1/5 genome-wide chromatin immunoprecipitation and sequencing (ChIP-seq) analyses of mESCs in the naïve or primed states, we revisit the roles of BMP signaling in mESCs. Overall design: RNA-seq analysis in 2 cell types; mESCs and ES-derived EpiSC (ESD-EpiSCs).

Publication Title

BMP Sustains Embryonic Stem Cell Self-Renewal through Distinct Functions of Different Krüppel-like Factors.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP154973
Reprogramming of Tumor-infiltrating Immune Cells in Early Stage of NSCLC
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Comparing the relative proportions of immune cells in tumor and adjacent normal tissue from NSCLC patients demonstrates the early changes of tumor immunity and provides insights to guide immunotherapy design. We mapped the immune ecosystem using computational deconvolution of bulk transcriptome data from the Cancer Genome Atlas (TCGA) and single cell RNA sequencing (scRNA-seq) data of dissociated tumors from early-stage non-small cell lung cancer (NSCLC) to investigate early immune landscape changes occurring during tumorigenesis. Computational deconvolution of immune infiltrates in 44 NSCLC and matching adjacent normal samples from TCGA showed heterogeneous patterns of alterations in immune cells. The scRNA-seq analyses of 11,485 cells from 4 treatment-naïve NSCLC patients comparing tumor to adjacent normal tissues showed diverse changes of immune cell compositions. Notably, CD8+ T cells and NK cells are present at low levels in adjacent normal tissues, and are further decreased within tumors. Myeloid cells exhibited marked dynamic reprogramming activities, which were delineated with differentiation paths through trajectory analysis. A common differentiation path from CD14+ monocytes to M2 macrophages was identified among the 4 cases, accompanied by up-regulated genes (e.g. ALCAM/CD166, CD59, IL13RA1, IL7R) with enriched functions (adipogenesis, lysosome), and down-regulated genes (e.g. CXCL2, IL1B, IL6R) with enriched functions (TNFa signaling via NF-kB, inflammatory response). Computational deconvolution and single cell sequencing analyses have revealed a highly dynamic immune reprogramming that occurs in early stage NSCLC development, suggesting that normalizing both immune compartments may represent a viable strategy for treatment of early stage cancer and prevention of progression. Overall design: Map the immune ecosystem using computational deconvolution of bulk transcriptome data from the Cancer Genome Atlas (TCGA) and single cell RNA sequencing (scRNA-seq) data of dissociated tumors from from early-stage non-small cell lung cancer (NSCLC) to investigate early immune landscape changes occurring during tumorigenesis

Publication Title

Dissecting intratumoral myeloid cell plasticity by single cell RNA-seq.

Sample Metadata Fields

Sex, Specimen part, Disease, Race, Subject

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accession-icon GSE68231
Expression data from human skeletal muscle
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The accumulation of intramyocellular lipid (IMCL) is recognized as an important determinant of insulin resistance, and is increased by a high-fat diet (HFD). However, the effects of HFD on IMCL and insulin sensitivity are highly variable.

Publication Title

Increased intramyocellular lipid/impaired insulin sensitivity is associated with altered lipid metabolic genes in muscle of high responders to a high-fat diet.

Sample Metadata Fields

Sex, Specimen part, Time

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accession-icon GSE9914
Expression data from early symptomatic Sca1154Q/2Q and Sca7266Q/5Q knock-in cerebellum
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Comparative analysis of cerebellar gene expression changes occurring in Sca1154Q/2Q and Sca7266Q/5Q knock-in mice

Publication Title

The insulin-like growth factor pathway is altered in spinocerebellar ataxia type 1 and type 7.

Sample Metadata Fields

Sex, Age

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accession-icon GSE61908
Early neuroinflammatory response precedes Purkinje cell loss in the cerebellum of SCA6 knockin mouse models
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Spinocerebellar ataxia type 6 (SCA6) is a dominantly inherited neurodegenerative disease caused by an expansion of a CAG repeat encoding a polyglutamine (PolyQ) tract in the Cav2.1 voltage-gated calcium channel. Pathologically, it is characterized by selective degeneration of cerebellar Purkinje cells (PCs), which are a common target for PolyQ-induced toxicity among several different SCAs. Mutant Cav2.1 confers toxicity mainly through a toxic gain-of-function mechanism, but subcellular site of expanded Cav2.1 toxicity is controversial and it remains elusive whether SCA6 shares pathogenic cascades with other SCAs. To gain insight into these problems, we studied the cerebellar gene expression patterns of young Sca6 MPI 118Q/118Q knockin (KI) mice, which express mutant Cav2.1 from endogenous locus and faithfully models human SCA6. Comparison of transcriptional changes with those of Sca1 154Q/2Q mice, a faithful KI mouse model of SCA1, revealed that transcriptional signatures in the MPI 118Q/118Q were distinct from those of Sca1 154Q/2Q. Examination of temporal profiles of candidate genes showed that upregulation of those associated with microglial activation was initiated before PC degeneration was apparent and augmented as the disease progressed. Histological analysis of the MPI 118Q/118Q cerebellum confirmed the presence of Iba-1 positive activated microglia. Moreover, predominance of M1-like pro-inflammatory microglia was observed and was concomitant with the increased expression of pro-inflammatory cytokines. These results suggest that the unique transcriptional response, which highlights upregulation of neuroinflammatory genes possibly associated with lysosomal involvement, may play a pivotal role in the pathogenesis. Modulation of innate immune system could pave the way for slowing the progression of SCA6.

Publication Title

Loss of MyD88 alters neuroinflammatory response and attenuates early Purkinje cell loss in a spinocerebellar ataxia type 6 mouse model.

Sample Metadata Fields

Specimen part

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accession-icon GSE76506
Leukocytes in non-tumor-bearing and tumor-bearing mice
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To clarify the functional role of migratory liver-resident leukocytes (LRLs) in the pre-metastatic lung, we identify differentially expressed genes and address biological significance in the liver.

Publication Title

Hepato-entrained B220<sup>+</sup>CD11c<sup>+</sup>NK1.1<sup>+</sup> cells regulate pre-metastatic niche formation in the lung.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE76235
LRL in liver and lung from tumor-stimulating mice.
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To understand the molecular mechanisms mediating Liver Resident Leukocytes (LRL) relocalization from the liver to the lungs in response to tumor progression, isolated LRLs from the liver and lungs of tumor-stimulating mice using a cell sorter. LRLs remaining in the liver displayed increased liver signature when compared to those that migrated into the lungs.

Publication Title

Hepato-entrained B220<sup>+</sup>CD11c<sup>+</sup>NK1.1<sup>+</sup> cells regulate pre-metastatic niche formation in the lung.

Sample Metadata Fields

Specimen part

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accession-icon GSE75690
Expression data from CD8alpha positive dendritic cells
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We screened a number of interferon inducible genes that may be involved in impeding HBV replication and found an anti-HBV activity in ISG20. ISG20 is an IFN-inducible 3- to 5-exonuclease, that degrades DNA and RNA and reduces antigen production in hepatocyte-derived cells

Publication Title

Interferon-stimulated gene of 20 kDa protein (ISG20) degrades RNA of hepatitis B virus to impede the replication of HBV in vitro and in vivo.

Sample Metadata Fields

Specimen part, 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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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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