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accession-icon E-MEXP-110
Transcription profiling of adult male whole MutaMouse lung with its immortalized 100% confluent epithelial lung cell line counterpart (Affymetrix)
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2), Affymetrix Murine Genome U74A Array (mgu74a)

Description

Biological comparison of gene expression profiles of adult male whole Muta™Mouse lung with its immortalized 100% confluent epithelial lung cell line counterpart. White, P.A.,et al. 2003. Development and characterization of an epithelial cell line from Muta™Mouse lung. Environ Mol Mutagen 42,3 pgs 166-184

Publication Title

Comprehensive comparison of six microarray technologies.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon GSE86643
Comparison of infloresence transcriptome of bp er vs. bp er fil
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

BP and ER encode proteins that act synergistically to regulate Arabidopsis inflorescence architecture. To search for genes/proteins that influence the BP/ER signaling pathways, we conducted mutagenesis of the bp er double mutant and found that a mutation in FILAMENTOUS FLOWER (FIL) suppresses many of the morphological/developmental defects in bp er. Given that FIL encodes a Zn-finger containing transcription factor, microarray analysis was conducted on bp er vs. the bp er fil line to identify genes that are misregulated and which might implicate specific genes/proteins/pathways that are involved in regulating inflorescence development.

Publication Title

A novel Filamentous Flower mutant suppresses brevipedicellus developmental defects and modulates glucosinolate and auxin levels.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE70271
caArray_jacks-00113: Murine KRASLA lung cancer gene expression
  • organism-icon Mus musculus
  • sample-icon 58 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Tumors from 5-6 month old KrasLA mice were dissected. Gene expression analysis on U74A affy chips. 19 normal lungs from age matched controls were also includeed

Publication Title

Comparison of gene expression and DNA copy number changes in a murine model of lung cancer.

Sample Metadata Fields

Sex, Age, Disease, Disease stage

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accession-icon GSE148325
Expression data for C. elegans blunt force trauma
  • organism-icon Caenorhabditis elegans
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Genome Array (celegans)

Description

C. elegans exhibit an age-dependent mechanical stress response to blunt force injury.

Publication Title

Trauma-induced regulation of VHP-1 modulates the cellular response to mechanical stress.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP117214
Angiogenic factor imbalance precedes complement deposition in the placenta of preeclamptic-like BPH/5 mice
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

BPH/5 mice are an inbred strain with “borderline hypertension” that spontaneously develops both maternal and fetal hallmarks of preeclampsia. RNA-Seq analysis of BPH/5 uterine implantation sites at embryonic day 7.5, the peak of decidualization, identifies differential expression of inflammatory response genes, including members of the complement family, compared to C57 controls. Overall design: RNA-Seq was performed on RNA isolated from E7.5 BPH/5 and C57 implantation sites (n=4).

Publication Title

Angiogenic factor imbalance precedes complement deposition in placentae of the BPH/5 model of preeclampsia.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon GSE12064
BMI-1 promotes Ewing sarcoma tumorigenicity independent of CDKN2a-repression
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Over-expression of the polycomb group gene BMI-1 is implicated in the pathogenesis of many human cancers. In this study, we investigate the role of BMI-1 as a functional oncogene in the Ewings Sarcoma Family of Tumors (ESFT), a highly aggressive group of bone and soft tissue tumors. Our data show that BMI-1 is highly expressed by the majority of primary ESFT and ESFT cell lines. However, in contrast to previous reports in other human cancer cell types, knockdown of BMI-1 in ESFT cell lines has no effect on cell survival. Instead, gain and loss of function studies in vitro and in vivo demonstrate that BMI-1 promotes the anchorage independent growth and tumorigenicity of ESFT. Importantly, we also find that modulation of BMI-1 alters the tumorigenicity of both p16-wild type and p16-null cell lines and that BMI-1-mediated effects on growth promotion are independent of CDKN2a repression. Gene expression profiling of ESFT cells following BMI-1 modulation reveals novel downstream effectors of BMI-1 function including key developmental, cell:cell and cell:matrix adhesion pathways. These data support a central role for BMI-1 in the pathogenesis of ESFT and reveal that p16-independent functions of BMI-1 are largely responsible for its oncogenic function in this tumor family.

Publication Title

BMI-1 promotes ewing sarcoma tumorigenicity independent of CDKN2A repression.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP149081
Dietary fat, but not dietary protein or carbohydrate (sucrose), regulates energy intake and causes adiposity in mice
  • organism-icon Mus musculus
  • sample-icon 95 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Purpose: Obesity is a global health issue. To investigate if protein and fat contents of the diets had effects on energy balance via the canonical hunger signaling pathways in the hypothalamus, RNAseq was performed on RNA extracted from the hypothalami of mice exposed to the different diets. A suggested mechanism by which animals may avoid obesity is by burning off excess energy via upregulation of white adipose tissue (WAT) browning. To investigate if protein and fat content of the diet had effects on energy balance via the browning related signaling pathways in the WAT, RNAseq was performed on RNA extracted from the subcutaneous WAT (sWAT) and epididymal WAT (eWAT) of mice exposed to the different diets. Methods: C57BL/6 male mice were used in this work. All mice were fed a standard diet with 10% fat and 20% protein (D12450B, Research Diets Ltd) for 2 weeks as the baseline period. Following 2 weeks of baseline monitoring (at age 12 weeks), all mice were randomly allocated to different groups and switched to the experimental diets for 12 weeks. After 12 weeks all mice were sacrificed and dissected. Methods: In total, mice were fed on 4 diet series, each series consisting of 6 different diets (total = 24 diets). In the first two series (Series 1: D14071601–D14071606 and series 2: D14071607 – D14071612) we fixed the level of fat by energy, and varied the protein content. The protein source was casein. The balance was made up by carbohydrate (roughly equal mix of corn starch and maltodextrose). The source of fat was a mix of cocoa butter, coconut oil, menhaden oil, palm oil and sunflower oil. This mix was designed to match the balance of saturated, mono-unsaturated and polyunsaturated fats (ratio 47.5: 36.8: 15.8) and the n-6: n-3 ratio (14.7: 1) in the typical western diet. The proportions of the different fat constituents and hence fatty acid distributions did not change as the total fat content changed. Sucrose and cellulose were both fixed 5% by energy and weight respectively, and all diets were supplemented with a standard vitamin and mineral mix. In the second two series of diets (series 3: D14071613 – D14071618 and series 4: D14071619 – D14071624) we fixed the level of protein by energy and then allowed the fat content to vary. In these diets the sucrose, cellulose and vitamin and mineral contents were the same as the diets in series 1 and 2. All these diets can be ordered direct from research diets (www.researchdiets.com) using the diet codes provided. Methods: From each diet group, the hypothalami of 8/20 individuals were collected. The left halves of two, and the right halves of another two, were pooled together as one sample, and the same was performed with the other 4 hypothalami, resulting in each diet group having 2 pooled samples of 4 hypothalami (n = 48 samples in total across 24 diets). From each diet group, the sWAT and eWAT of 12/20 individuals were also collected. A small piece from each of six sWAT collections were pooled together as one sample, and the same was performed with the other six eWAT collections. In this way each diet group had one pooled sWAT sample and one pooled eWAT sample (also n = 48 across 24 diets). Methods: The total RNA of the hypothalamus and WAT was isolated using the RNeasy Mini Kit (QIAGEN, 74104) according to manufacturer''s protocol. All sequencing was carried out using the Illumina NextSeq 500 sequencer. RNA fragments were sequenced by 75 bp long reads from paired ends (PE 2 x 75 bp, 150 bp per fragment). Quality control checks for raw data FASTQ files were done by using FASTQC (a quality control tool for high throughput sequence data; http://www.bioinformatics.babraham.ac.uk/projects/fastqc/). Paired-end reads were mapped to the Mus musculus genome (GRCm38) using Bowtie 2-2.1.0, TopHat-2.0.10, and Samtools-0.1.19; uniquely mapped reads for each gene were counted against the GTF file of GRCm38 provided by Ensembl (release 83) using HTSeq-0.6.1p1 using the strand = reverse; after read count data were obtained from the TopHat-HTSeq pipeline, counts per million (CPM) value for each gene was calculated by using the R package 'edgeR' (version 3.12.0, R version 3.2.2) to normalize the count data by the size of the library of each sample. Genes with the CPM value = 1 in at least one of the 24 diets group were retained (Anders et al., 2013). Generalized Linear Modelling (GLM) was applied by R (version 3.2.2). The GLM model used here was: ~p+f+p:f, which regresses gene expression (CPM) against the protein (p) and fat contents (f) of diets, as well as their interaction (p:f). However, when the effect of the interaction was not significant (p value = 0.05), the interaction term was dropped and a revised model (~p+f) was utilized. Results: With TopHat-HTSeq pipeline, reads of each sample were mapped to 46,078 genes. In hypothalamus there were 15,371 genes with the counts per million (CPM) value = 1 in at least one of the 24 diets group; in white adipose tissue there were 18,202 genes with the CPM value = 1 in at least one of the 24 diets group. No major changes in hypothalamic gene expression levels were found in relation to different dietary protein levels at fixed fat contents, however hypothalamic gene expression showed increase in expression of genes in reward pathways in relation to dietary fat, while Agrp and Npy were both downregulated in relation to dietary fat levels. WAT gene expression showed decrease in expression of general thermogenic related genes and WAT browning related genes in relation to both dietary protein and dietary fat, while Tgfb1, Pdk4 and Fgf1 were all upregulated in relation to dietary fat levels. Conclusions: Significant positive associations were evident between the fat levels of the diet and the main hedonic signaling systems linked to food intake. Significant negative associations were found between both protein and fat levels of the diet and WAT browning or general thermogenic signalings linked to energy expenditure. Overall design: In total 96 samples are analyzed. From each diet group, the hypothalami of 8/20 individuals were collected. The left halves of two, and the right halves of another two, were pooled together as one sample, and the same was performed with the other 4 hypothalami, resulting in each diet group having 2 pooled samples of 4 hypothalami (n = 48 samples in total across 24 diets). From each diet group, the sWAT and eWAT of 12/20 individuals were also collected. A small piece from each of six sWAT collections were pooled together as one sample, and the same was performed with the other six eWAT collections. In this way each diet group had one pooled sWAT sample and one pooled eWAT sample (also n = 48 across 24 diets)

Publication Title

Dietary Fat, but Not Protein or Carbohydrate, Regulates Energy Intake and Causes Adiposity in Mice.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, Subject

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accession-icon GSE71258
Identification of genes associated with breast cancer micrometastatic disease in bone marrow disseminated tumor cells (DTCs)
  • organism-icon Homo sapiens
  • sample-icon 126 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In this study, we assess the effect of zoledronic acid on clearance of disseminated tumour cells (DTCs) from the bone marrow in women undergoing neoadjuvant chemotherapy for breast cancer

Publication Title

CXCR4 Protein Epitope Mimetic Antagonist POL5551 Disrupts Metastasis and Enhances Chemotherapy Effect in Triple-Negative Breast Cancer.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE76630
Stromal-Based Signatures for the Classification of Gastric Cancer
  • organism-icon Mus musculus
  • sample-icon 98 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Stromal-Based Signatures for the Classification of Gastric Cancer.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE76628
Stromal-Based Signatures for the Classification of Gastric Cancer [part II]
  • organism-icon Mus musculus
  • sample-icon 78 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Increasing success is being achieved in the treatment of malignancies with stromal-targeted therapies, predominantly in anti-angiogenesis and immunotherapy, predominantly checkpoint inhibitors. Despite 15 years of clinical trials with anti-VEGF pathway inhibitors for cancer, we still find ourselves lacking reliable predictive biomarkers to select patients for anti-angiogenesis therapy. For the more recent immunotherapy agents, there are many approaches for patient selection under investigation. Notably, the predictive power of an Ad-VEGF-A164 mouse model to drive a stromal response with similarities to a wound healing response shows relevance for human cancer and was used to generate stromal signatures. We have developed gene signatures for 3 stromal states and leveraged the data from multiple large cohort bioinformatics studies of gastric cancer (TCGA, ACRG) to further understand how these relate to the dominant patient phenotypes identified by previous bioinformatics efforts. We have also designed multiplexed IHC assays that robustly represent the vascular and immune diversity in gastric cancer. Finally, we have used this methodology to arrive at a hypothesis of how angiogenesis and immunotherapy may fit into the experimental approaches for gastric cancer treatments.

Publication Title

Stromal-Based Signatures for the Classification of Gastric Cancer.

Sample Metadata Fields

Sex, Specimen part

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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