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accession-icon GSE23603
Gene expression in ovarian cancer
  • organism-icon Homo sapiens
  • sample-icon 59 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

BAD phosphorylation determines ovarian cancer chemosensitivity and patient survival.

Sample Metadata Fields

Disease stage, Cell line

View Samples
accession-icon GSE23553
Gene expression changes with induction of in-vitro platinum-resistance in ovarian cancer cell lines.
  • organism-icon Homo sapiens
  • sample-icon 38 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

We treated 8 human ovarian cancer cell lines with cisplatin in treatment/recovery cycles to induce in-vitro resistance to the drug. Microarrays measured gene expression at baseline and after each dose schedule (after recovery).

Publication Title

BAD phosphorylation determines ovarian cancer chemosensitivity and patient survival.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE23554
Ovarian Cancer Dataset
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Background. Genome-wide expression changes are associated with development of chemoresistance in patients with ovarian cancer (OVCA); the BCL2 antagonist of cell death (BAD) apoptosis pathway may play a role in clinical outcome.

Publication Title

BAD phosphorylation determines ovarian cancer chemosensitivity and patient survival.

Sample Metadata Fields

Disease stage

View Samples
accession-icon GSE73044
Expression data from prostate cancer and osteoblast co-cultures
  • organism-icon Homo sapiens, Rattus norvegicus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Dynamic interaction between prostate cancer and the bone microenvironment is a major contributor to metastasis of prostate cancer to bone. In this study we utilized an in-vitro co-culture model of PC3 prostate cancer cells and osteoblasts followed by microarray based gene expression profiling to identify previously unrecognized prostate cancer-bone microenvironment interactions. Factors secreted by PC3 cells resulted in the up-regulation of many genes in osteoblasts associated with bone metabolism and cancer metastasis, including Mmp13, Il-6 and Tgfb2, and down-regulation of Wnt inhibitor Sost. To determine whether altered Sost expression in the bone microenvironment has an effect on prostate cancer metastasis, we co-cultured PC3 cells with Sost knockout (SostKO) osteoblasts and wildtype (WT) osteoblasts and identified several genes differentially regulated between PC3-SostKO osteoblast co-cultures and PC3-WT osteoblast co-cultures. Co-culturing PC3 cells with WT osteoblasts up-regulated cancer-associated long noncoding RNA (lncRNA) MALAT1 in PC3 cells. MALAT1 expression was further enhanced when PC3 cells were co-cultured with SostKO osteoblasts and treatment with recombinant Sost down-regulated MALAT1 expression in these cells. Our results suggest that reduced Sost expression in the tumor microenvironment may promote bone metastasis by up-regulating MALAT1 in prostate cancer.

Publication Title

Cancer-Osteoblast Interaction Reduces Sost Expression in Osteoblasts and Up-Regulates lncRNA MALAT1 in Prostate Cancer.

Sample Metadata Fields

Cell line

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accession-icon GSE24509
Expression of microRNAs and their gene targets are dysregulated in pre-invasive breast cancer
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Expression of microRNA and their gene targets are dysregulated in preinvasive breast cancer.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

View Samples
accession-icon GSE24506
Expression of microRNAs and their gene targets are dysregulated in pre-invasive breast cancer (mRNA)
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Introduction: microRNAs (miRNAs) are short non-coding RNAs that negatively regulate gene expression and may play a causal role in invasive breast cancer. Since many genetic aberrations of invasive disease are detectable in earlier stages, we hypothesized that miRNA expression dysregulation and the predicted changes in gene expression would also be found in early breast neoplasias. Methods: Expression profiling of 365 miRNAs by RT-qPCR was combined with laser-capture microdissection to obtain an epithelial specific miRNA expression signature of normal breast epithelium (n=9) and of paired samples of histologically normal epithelium (HN) and ductal carcinoma in situ (DCIS) (n=16). To determine how miRNAs may control the expression of co-dysregulated mRNAs we also performed gene expression microarray analysis in the same paired HN and DCIS samples and integrated this with miRNA-target prediction. We further validated several target pairs by modulating the expression levels of miRNAs in MCF7 cells and measured the expression of target mRNAs and proteins. Results: Thirty-five miRNAs were aberrantly expressed between RM, HN and DCIS. Twenty-nine miRNAs and 420 mRNAs were aberrantly expressed between HN and DCIS. Combining these two datasets with miRNA-target prediction we identified two established target pairs (miR-195:CCND1 and miR-21:NFIB) and tested several novel miRNA:mRNA target pairs. Over-expression of the putative tumor-suppressor miR-125b, under-expressed in DCIS, repressed the expression of MEMO1, which is required for ErbB2-driven cell motility (also a target of miR-125b); and NRIP1/RIP140, which modulates the transcriptional activity of the estrogen receptor. Knockdown of the putative oncogenic miRNAs miR-182 and miR-183, both highly over-expressed in DCIS, increased the expression of CBX7 (which regulates E-cadherin expression), DOK4, NMT2, and EGR1. Augmentation of CBX7 by knockdown of miR-182 expression, in turn, positively regulated the expression of E-cadherin, a key protein involved in maintaining normal epithelial cell morphology which is commonly lost during neoplastic progression. Conclusions: These data provide the first miRNA expression profile of normal breast epithelium and of pre-invasive breast carcinoma. Further, we demonstrate that altered miRNA expression can modulate gene expression changes that characterize these early cancers. We conclude that miRNA dysregulation likely plays a substantial role in early breast cancer development.

Publication Title

Expression of microRNA and their gene targets are dysregulated in preinvasive breast cancer.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

View Samples
accession-icon GSE7895
Reversible and Permanent effects of Tobacco Smoke Exposure on Airway Epithelial Gene Expression
  • organism-icon Homo sapiens
  • sample-icon 104 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

RNA was obtained from histologically normal bronchial epithelium of never, former, and current smokers undergoing fiberoptic bronchoscopy.

Publication Title

Reversible and permanent effects of tobacco smoke exposure on airway epithelial gene expression.

Sample Metadata Fields

Age

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accession-icon GSE98595
Cabergoline-treated lutein granulosa cells from polycystic ovarian syndrome (PCOS) patients exhibit higher transcriptomic response than cabergoline-treated controls
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This study assessed the transcriptomic profiles of lutein granulosa cells (LGCs) from women with and without PCOS using Affymetrix microarray chips to provide novel information about the molecular changes that occur in these cells when they are treated with a D2-ag (Cb2) and to assess the signal transduction pathways regulated by this treatment.

Publication Title

Dysregulated genes and their functional pathways in luteinized granulosa cells from PCOS patients after cabergoline treatment.

Sample Metadata Fields

Specimen part, Disease

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accession-icon SRP021101
Global transcriptome profiling of Oct4/Klf4/Sox2 (3Factor, 3F) + IL6 iPS clones derived from mouse embryonic fibroblasts.
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We used heterokaryon cell fusion based reprogramming and identified the cytokine IL6 as a potential regulator of reprogramming to pluripotency. We generated iPS clones using the four reprogramming factors (4F) Oct4, Klf4, Sox2, and c-Myc. In addition, iPS clones were generated using only three factors (3F: Oct4, Klf4, amd Sox2) with the addition of the cytokine IL6 to reprogramming culture conditions. Global RNA-Seq of the 3F + IL6 derived iPS clones was done for comparison with 4F-derived iPS clones, mouse embryonic stem cells and mouse embryonic fibroblasts. Overall design: This study includes 8 samples: 2 independently derived 3F + IL6 iPS clones, 2 independently derived 4F iPS clones, 2 biological replicates of mouse D3-GFP ES cells, and 2 biological replicates of mouse embryonic fibroblasts (MEFs). The latter 6 samples are provided as references for the 3F + IL6 iPS clones. Poly-A RNA was isolated and prepared for sequencing using the Illumina TruSeq RNA kit (v2) to generate 50bp reads. Reads were aligned to mm10.

Publication Title

NKX3-1 is required for induced pluripotent stem cell reprogramming and can replace OCT4 in mouse and human iPSC induction.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon SRP137014
Comparative Transcriptomics of STR/ort, C57BL/6 and MRL/MpJ Knee Joints
  • organism-icon Mus musculus
  • sample-icon 100 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Injuries to the anterior cruciate ligament (ACL) often result in post-traumatic osteoarthritis (PTOA). PTOA accounts for ~12% of all osteoarthritis (OA) cases, yet the mechanisms contributing to OA after joint injury are not well understood. To better understand the molecular mechanisms behind PTOA development following ACL injury, we profiled ACL injury-induced gene expression changes in knee joints of three mouse strains with varying susceptibility to PTOA: STR/ort (highly susceptible), C57BL/6 (moderately susceptible) and super-healer MRL/MpJ (not susceptible) and identified genes differentially expressed between these strains at 0-day [before injury], 1-day, 1-week, and 2-weeks post-injury. This study highlights many new potential therapeutic targets and OA biomarkers. Overall design: Comparative transcriptomics to understand the molecular changes associated with early stages of PTOA development in STR/ort, C57BL/6 and MRL/MpJ mice and to identify genes that contribute to increased OA susceptibility in STR/ort and resistance to PTOA in MRL/MpJ.

Publication Title

Comparative Transcriptomics Identifies Novel Genes and Pathways Involved in Post-Traumatic Osteoarthritis Development and Progression.

Sample Metadata Fields

Age, Specimen part, Cell line, Treatment, Subject

View Samples
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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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