refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 55 results
Sort by

Filters

Technology

Platform

accession-icon GSE52129
Gene expression profile of activated CD4 T cells from adults and newborns
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Given their precipitous encounter with the environment, newborn infants might be expected to possess abundant immunoprotective mechanisms. Paradoxically, their T cells display grossly impaired Th1 anti-bacterial and anti-viral responses. This study identifies factors produced by neonatal CD4 T cells when compared with adult naive CD4 T cells and highlights CXCL8 as a pivotal effector molecule in neonatal T cells. Using Affimetrix microarray we compared gene expression in cord blood derived CD4 T cells with naive CD4 T cells from adults after polyclonal stimulation.

Publication Title

Interleukin-8 (CXCL8) production is a signatory T cell effector function of human newborn infants.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE110811
Distinct Gene Expression Profiles Define Anaplastic Grade in Retinoblastoma
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Morbidity and mortality associated with retinoblastoma have decreased drastically in recent decades, in large part due to better prediction of high-risk disease and appropriate treatment stratification. High-risk histopathologic features and severe anaplasia both predict the need for more aggressive treatment; however, not all centers are able to easily assess tumor samples for degree of anaplasia. Instead, identification of genetic signatures able to distinguish among anaplastic grades and thus predict high versus low risk retinoblastoma would facilitate appropriate risk stratification in a wider patient population. A better understanding of genes dysregulated in anaplasia would also yield valuable insights into pathways underlying the development of more severe retinoblastoma. Here, we present the histopathologic and gene expression analysis of 28 retinoblastoma cases using microarray analysis. Tumors of differing anaplastic grade show clear differential gene expression, with significant dysregulation of unique genes and pathways in severe anaplasia. Photoreceptor and nucleoporin expression in particular are identified as highly dysregulated in severe anaplasia and suggest particular cellular processes contributing to the development of increased retinoblastoma severity. A limited set of highly differentially expressed genes are also able to accurately predict severe anaplasia in our dataset. Together, these data contribute to the understanding of the development of anaplasia and facilitate the identification of genetic markers of high-risk retinoblastoma.

Publication Title

Distinct Gene Expression Profiles Define Anaplastic Grade in Retinoblastoma.

Sample Metadata Fields

Specimen part

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

View Samples
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

View Samples
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

View Samples
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

View Samples
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
accession-icon GSE56704
Densely Ionizing Radiation Effects on the Microenvironment Promote Aggressive Trp53 Null Mammary Carcinomas
  • organism-icon Mus musculus
  • sample-icon 44 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Densely ionizing radiation is a major component of the space radiation environment and has potentially greater carcinogenic effect compared to sparsely ionizing radiation that is prevalent in the terrestrial environment. It is unknown to what extent the irradiated microenvironment contributes to the differential carcinogenic potential of densely ionizing radiation. To address this gap, 10-week old BALB/c mice were irradiated with 100 cGy sparsely ionizing g-radiation or 10, 30, or 80 cGy of densely ionizing, 350 MeV/amu Si particles and transplanted 3 days later with syngeneic Trp53 null mammary fragments. Tumor appearance was monitored for 600 days. Tumors arising in Si-particle irradiated mice had a shorter median time to appearance, grew faster and were more likely to metastasize. Most tumors arising in sham-irradiated mice were ER-positive, pseudo-glandular and contained both basal keratin 14 and luminal keratin 8/18 cells (designated K14/18), while most tumors arising in irradiated hosts were K8/18 positive (designated K18) and ER negative. Comparison of K18 vs K14/18 tumor expression profiles showed that genes increased in K18 tumors were associated with ERBB2 and KRAS while decreased genes overlapped with those down regulated in metastasis and by loss of E-cadherin. Consistent with this, K18 tumors grew faster than K14/18 tumors and more mice with K18 tumors developed lung metastases compared to mice with K14/18 tumors. However, K18 tumors arising in Si-particle irradiated mice grew even faster and were more metastatic compared to control mice. A K18 Si-irradiated host profile was enriched in genes involved in mammary stem cells, stroma, and Notch signaling. Thus systemic responses to densely ionizing radiation enriches for a ER-negative, K18-positive tumor, whose biology is more aggressive compared to similar tumors arising in non-irradiated hosts.

Publication Title

Densely ionizing radiation acts via the microenvironment to promote aggressive Trp53-null mammary carcinomas.

Sample Metadata Fields

No sample metadata fields

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact