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accession-icon GSE7741
Expression data of HCV-associated advance disease state
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Introduction: Mechanisms that contribute to the pathogenesis of liver damage caused by hepatitis C virus (HCV) are not fully understood. Our previous work on liver biopsies from chronic HCV patients has shown modulation of the expression of certain cell cycle proteins indicating HCV-induced modifications of cell cycle events. We therefore hypothesize that HCV infection disrupts normal regulation of cell cycle that contributes to disease progression. Objective: To identify molecular disruptions during the course of HCV-associated disease progression, using liver biopsy specimens of chronic hepatitis C patients. Methods: Liver biopsy samples classified on histological basis as early (fibrosis stage 0-1) or advanced (fibrosis stage 3-4) disease stage were studied using oligonucleotide array ( HG U133 Plus 2.0, Affymetrix GeneChip System). For comparison, liver specimens from patients with non-viral hepatitis were also analyzed by microarray. Expression data was analyzed using Genespring (GX 7.2) and Ingenuity Pathway analysis (3.0). The differential expression of selected cell cycle genes (cyclin D2, KPNA2, HERC5 and Bcl-2) identified after microarray analysis was confirmed by quantitative real-time RT-PCR. Results: Microarray analysis revealed two-fold or greater transcriptional change in 792 genes of the total 38,500 known human genes in HCV-advance disease stage (HCV-A) as compared to HCV-early disease stage (HCV-E). Most of the genes have a defined role in immune response, extracellular matrix and cell cycle and apoptosis.

Publication Title

Gene profiling of early and advanced liver disease in chronic hepatitis C patients.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon SRP080859
RNA-seq reveals changes in the astrocyte transcriptome following Borrelia burgdorferi infection
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

mRNA profiles of astrocytes infected with Borrelia burdorferi for 24 hours, 48 hours, and 24 hour uninfected controls were generated by deep sequencing, in triplicate, using Illumina HiSeq. Overall design: mRNA profiles of astrocytes infected with Borrelia burdorferi for 24 hours, 48 hours, and 24 hour uninfected controls were generated by deep sequencing, in triplicate, using Illumina HiSeq.

Publication Title

MicroRNA and mRNA Transcriptome Profiling in Primary Human Astrocytes Infected with Borrelia burgdorferi.

Sample Metadata Fields

Specimen part, Subject, Time

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accession-icon SRP192094
Disease modelling of core pre-mRNA splicing factor haploinsufficiency
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

We generated a human EFTUD2 knockdown cell line using a CRISPR cas9 nickase strategy to investigate the effects of decreased expression of core spliceosome components on cell characteristics and global transcriptome expression/splicing patterns Overall design: 6 biological replicates of WT or CRISPR knock-down cells were generated and analysed by RNA-Seq

Publication Title

Disease modeling of core pre-mRNA splicing factor haploinsufficiency.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE80236
Identification of miR-210 target genes in T20 patient-derived sphere culture
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Hypoxia is known to regulate tumor-initiating cells and to have an effect on miRNA expression. We were interested in studying the role of hypoxia-induced miR-210 in colorectal cancer patient-derived sphere cultures.

Publication Title

Hypoxia-responsive miR-210 promotes self-renewal capacity of colon tumor-initiating cells by repressing ISCU and by inducing lactate production.

Sample Metadata Fields

Specimen part

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accession-icon GSE89524
Identification of differentially expressed miRNAs between SW480 and SW620 spheroid cultures
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The miR-371∼373 Cluster Represses Colon Cancer Initiation and Metastatic Colonization by Inhibiting the TGFBR2/ID1 Signaling Axis.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE89523
Identification of differentially expressed genes between SW480 and SW620 spheroid cultures [mRNA]
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

The colorectal cancer (CRC) cell line pair SW480/SW620 is an accepted model to study CRC progression and metastasis formation. Studying gene expression differences might allow to uncover molecular mechanisms that underlie metastasis initiation

Publication Title

The miR-371∼373 Cluster Represses Colon Cancer Initiation and Metastatic Colonization by Inhibiting the TGFBR2/ID1 Signaling Axis.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP051333
Effect of PDZ domain binding Kinase inhibition using TOPK-32 (called PBKi) on C4-2 cell transcriptome
  • organism-icon Homo sapiens
  • sample-icon 48 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Analysis of C4-2 prostate cancer cell line after 6 hrs of treatment with TOPK-32. PBK is overexpressed in a number of solid tumours, including prostate cancer. Results provide insight into the molecular mechanisms of PBK in prostate carcinogenesis. Overall design: This experiment was designed to understand the regulation of transcriptome by PDZ domain binding kinase, which is an important kinase with role in cell cycle. The cells were treated with a catalytic inhibitor TOPK32 which inhibits the kinase activity of PBK protein.

Publication Title

A reciprocal feedback between the PDZ binding kinase and androgen receptor drives prostate cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP050332
Effect of PBK knockdown on C4-2 cell transcriptome
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Analysis of C4-2 Prostate cancer cell line after 72 hours of knockdown. PBK is overexpressed in a number of solid tumours, including prostate cancer. Results provide insight into the molecular mechanisms of PBK in prostate carcinogenesis. Overall design: This experiment was designed to understand the regulation of transcriptiome by PDZ domain binding kinase (PBK), which is an important kinase with role in cell cycle. In order to achieve this, the endogenous protein was knocked down using siRNA pool that targets the PBK mRNA.

Publication Title

A reciprocal feedback between the PDZ binding kinase and androgen receptor drives prostate cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP050331
Effect of CHKA knockdown on C4-2 cell transcriptome
  • organism-icon Homo sapiens
  • sample-icon 48 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Analysis of C4-2 Prostate cancer cell line after 72 hours of knockdown. CHKA is overexpressed in a number of solid tumours, including prostate cancer. Results provide insight into the molecular mechanisms of CHKA in prostate carcinogenesis. Overall design: This experiment was designed to understand the regulation of transcriptome by Choline kinase alpha (CHKA) which is an important enzyme in Kennedy pathway. In order to achieve this, the endogenous protein was knocked down using siRNA pool that targets the CHKA mRNA.

Publication Title

Choline Kinase Alpha as an Androgen Receptor Chaperone and Prostate Cancer Therapeutic Target.

Sample Metadata Fields

No sample metadata fields

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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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