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accession-icon GSE75535
Gene expresssion profiles of cancer of the appendix
  • organism-icon Homo sapiens
  • sample-icon 63 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Appendiceal cancer patients treated with cytoreductive surgery (CRS) and hyperthermic intraperitoneal chemotherapy (HIPEC) often demonstrate an unpredictable variability in survival outcomes. Biomarkers predictive of CRS/HIPEC efficacy could better guide treatment decisions. In this study we hypothesized that variation in the transcriptional programming of appendiceal tumors might distinguish molecular subtypes with differential outcomes after CRS/HIPEC. The goal of this study was to investigate the potential of a prognostic gene signature to discriminate patients with favorable and unfavorable outcomes in a discovery set of patient (the original tumor series (n=24)), and confirm its prognostic value in a second validation series (the validation cohort (n=39)).

Publication Title

Prognostic Molecular Subtypes of Low-Grade Cancer of the Appendix.

Sample Metadata Fields

Sex, Age

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accession-icon GSE27272
Comprehensive Study of Tobacco Smoke-Related Transcriptome Alterations in Maternal and Fetal Cells
  • organism-icon Homo sapiens
  • sample-icon 183 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip

Description

Maternal smoking has a severe negative effect on all stages of pregnancy that in consequence impairs fetal growth and development. Tobacco smoke-related defects are well established at the clinical level; however, little is known about molecular mechanisms underlying these pathological conditions. We thus employed a genomic approach to determine transcriptome alterations induced by maternal smoking in pregnancy. We assayed gene expression profiles in peripheral blood (M) leukocytes and placentas (PL) of pregnant smokers and those without significant exposure, and in cord blood (D) leukocytes of their babies. Comparative analyses defined significant deregulation of 193 genes in M cells, 329 genes in placentas, and 49 genes in D cells of smokers. These genes were mainly involved in xenobiotic metabolism, oxidative stress, inflammation, immunity, hematopoiesis, trophoblast differentiation, and vascularization. Functional annotation of the deregulated genes outlined processes and pathways affected by tobacco smoke. In smoker newborns, we identified several deregulated pathways associated with autoimmune diseases. The study demonstrates a limited ability of placenta to modulate toxic effects of maternal tobacco use at the gene expression level.

Publication Title

Transcriptome alterations in maternal and fetal cells induced by tobacco smoke.

Sample Metadata Fields

Age, Specimen part, Subject

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accession-icon GSE30032
Deregulation of Gene Expression induced by Environmental Tobacco Smoke Exposure in Pregnancy
  • organism-icon Homo sapiens
  • sample-icon 104 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip

Description

Passive smoke intake by pregnant women may have detrimental effects such as spontaneous abortion, lower birth weight, stillbirth, and reduced infant lung function. To extend our knowledge on molecular effects of tobacco smoke exposure in pregnancy, we analyzed transcriptome alterations in passive smokers (PS) and compared them to those in active smokers (AS). Using Illumina Expression Beadchip with 24,526 transcript probes, gene expression patterns were assayed in placentas from PS (N=25) exposed to environmental tobacco smoke (ETS) throughout pregnancy and non-exposed (NS) counterparts (N=35), and in cord blood cells from their newborns. The ETS exposure was evaluated by questionnaire disclosure and cotinine measurement in maternal and cord bloods. A total of 196 genes were significantly deregulated in placentas of PS compared to NS. These genes were primary associated with extracellular matrix, apoptosis, blood clotting, response to stress, embryonic morphogenesis, and lipid metabolism. Cord blood of newborns of PS displayed differential expression of 116 genes encoding mainly neuronal factors, regulators of immunologic response, and protooncogenes. Gene ontology analyses highlighted some important biological processes that might be associated with placental insufficiency and fetal growth restriction in PS, such as fatty acid catabolism, coagulation, regulation of growth, and response to steroid hormone stimulus. The study demonstrates that even low dose exposure to ETS during pregnancy leads to the significant deregulation of transcriptional regulation in placental and fetal cells. The data suggest the effect of ETS on the fetus is primary indirect, mediated via deregulation of placental functions. Comparison of PS and AS indicated that ETS exposure and active smoking in pregnancy partly employ the same molecular mechanisms.

Publication Title

Deregulation of gene expression induced by environmental tobacco smoke exposure in pregnancy.

Sample Metadata Fields

Age

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accession-icon SRP113227
Sequencing of tumor associated (B16f10-OVA) mir-155 Wt or deficient CD4+ and CD8+ T cells
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Tumor associated CD4+ and CD8+ T cells were sorted from B16f10 OVA expressing tumors in miR-155 flox, miR-155 flox CD4Cre+, and miR-155 flox CD4Cre+ mice treated with immune checkpoint blocking (ICB) antibodies by flow sorting on CD45+CD3+CD4+ cells and CD45+ CD3+CD8+ cells. RNA was collected from these cells to perform RNA sequencing of total RNA. Overall design: Each sample represents cells from 2 to 3 individual tumors grown on individual mice that were pooled together before sorting via flow cytometry

Publication Title

Antitumor immunity is defective in T cell-specific microRNA-155-deficient mice and is rescued by immune checkpoint blockade.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP087467
Expression profile of hematopoietic stem and progenitor cell (HSPC) compartment of FLT3-ITD and FLT3-ITD miR-155-/- mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The miR-155-dependent differences in gene expression in the HSPC compartment of FLT3-ITD mice is unknown. In this experiment, we performed RNA sequencing on FLT3-ITD and FLT3-ITD miR-155-/- mouse LKS cells. Overall design: RNA sequencing was performed on RNA extracted from Lin-, cKit+, Sca1+ cells isolated via flow cytometry from FLT3-ITD and FLT3-ITD miR-155-/- mice. 3 samples were submitted for sequencing for each experimental group. Each sample contains RNA from 3 mice, in order to get enough RNA from this rare stem cell population.

Publication Title

miR-155 promotes FLT3-ITD-induced myeloproliferative disease through inhibition of the interferon response.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP160877
Sequencing of F4/40+ CD11b+ macrophages from adipose tissue of miR-146a WT or deficient mice on high fat or normal chow diet
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We identify regulatory mechanisms that influence inflammation and metabolism during metabolic disease development. In addition to the other data represented in our paper, we performed RNA-seq to demonstrate a role for miR-146a, an anti-inflammatory miRNA, in regulating both inflammation and cellular metabolism during obesity. Overall design: Each sample represents pooled cells from three mice of the same genotype and treatment group. Samples were pooled before FACS to ensure sufficient cell numbers for sorting and RNA collection. WT or miR-146a-/- mice were treated with either high fat diet or normal chow diet for 14 weeks starting from 6 weeks of age. Mice were sacrificed and live, singlet CD45+ CD11b+ F4/80+ cells were sorted from the stromal vascular fraction of adipose tissue using FACS Aria. RNA was collected from the sorted cells via Qiazol/RNeasy Kit (Qiagen) and library preparation used Illumina TruSeq Stranded RNA Kit with Ribo-Zero Gold. RNA-seq was performed using Illumina HiSeq 50 cycle single-read sequencing version 4. Sequence alignment was performed through the University of Utah Bioinformatics Core Facility.

Publication Title

Anti-inflammatory microRNA-146a protects mice from diet-induced metabolic disease.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE116436
Drug-induced change in gene expression across NCI-60 cell lines after exposure to 15 anticancer agents for 2, 6 and 24h
  • organism-icon Homo sapiens
  • sample-icon 6633 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2), Affymetrix HT Human Genome U133A Array (hthgu133a)

Description

To identify patterns of drug-induced gene modulation that occur across different cell types, we measured gene expression changes across NCI-60 cell lines after exposure to 15 anticancer agents. The results were integrated into a database and set of interactive analysis tools, the NCI Transcriptional Pharmacodynamics Workbench (NCI TPW), intended to allow exploration of gene expression modulation, including by molecular pathway, drug target, and association with drug sensitivity. We identified common transcriptional responses across drugs and cell types and uncovered cell signaling pathway–specific gene expression changes associated with drug sensitivity. We also demonstrated the value of this tool for investigating clinically relevant molecular hypotheses, utilizing the NCI TPW to assess drug-induced expression changes in genes associated with immune function and epithelial-mesenchymal transition, and to identify candidate biomarkers for drug activity. The NCI TPW provides a comprehensive resource to facilitate understanding of tumor cell characteristics that define sensitivity to anticancer drugs.

Publication Title

The NCI Transcriptional Pharmacodynamics Workbench: A Tool to Examine Dynamic Expression Profiling of Therapeutic Response in the NCI-60 Cell Line Panel.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE116446
Drug-induced change in gene expression across NCI-60 cell lines after exposure to 15 anticancer agents for 2, 6 and 24h (paclitaxel)
  • organism-icon Homo sapiens
  • sample-icon 538 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Human Genome U133A Array (hthgu133a), Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

To identify patterns of drug-induced gene modulation that occur across different cell types, we measured gene expression changes across NCI-60 cell lines after exposure to 15 anticancer agents. The results were integrated into a database and set of interactive analysis tools, the NCI Transcriptional Pharmacodynamics Workbench (NCI TPW), intended to allow exploration of gene expression modulation, including by molecular pathway, drug target, and association with drug sensitivity. We identified common transcriptional responses across drugs and cell types and uncovered cell signaling pathwayspecific gene expression changes associated with drug sensitivity. We also demonstrated the value of this tool for investigating clinically relevant molecular hypotheses, utilizing the NCI TPW to assess drug-induced expression changes in genes associated with immune function and epithelial-mesenchymal transition, and to identify candidate biomarkers for drug activity. The NCI TPW provides a comprehensive resource to facilitate understanding of tumor cell characteristics that define sensitivity to anticancer drugs.

Publication Title

The NCI Transcriptional Pharmacodynamics Workbench: A Tool to Examine Dynamic Expression Profiling of Therapeutic Response in the NCI-60 Cell Line Panel.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE116442
Drug-induced change in gene expression across NCI-60 cell lines after exposure to 15 anticancer agents for 2, 6 and 24h (erlotinib)
  • organism-icon Homo sapiens
  • sample-icon 534 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Human Genome U133A Array (hthgu133a), Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

To identify patterns of drug-induced gene modulation that occur across different cell types, we measured gene expression changes across NCI-60 cell lines after exposure to 15 anticancer agents. The results were integrated into a database and set of interactive analysis tools, the NCI Transcriptional Pharmacodynamics Workbench (NCI TPW), intended to allow exploration of gene expression modulation, including by molecular pathway, drug target, and association with drug sensitivity. We identified common transcriptional responses across drugs and cell types and uncovered cell signaling pathwayspecific gene expression changes associated with drug sensitivity. We also demonstrated the value of this tool for investigating clinically relevant molecular hypotheses, utilizing the NCI TPW to assess drug-induced expression changes in genes associated with immune function and epithelial-mesenchymal transition, and to identify candidate biomarkers for drug activity. The NCI TPW provides a comprehensive resource to facilitate understanding of tumor cell characteristics that define sensitivity to anticancer drugs.

Publication Title

The NCI Transcriptional Pharmacodynamics Workbench: A Tool to Examine Dynamic Expression Profiling of Therapeutic Response in the NCI-60 Cell Line Panel.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE116451
Drug-induced change in gene expression across NCI-60 cell lines after exposure to 15 anticancer agents for 2, 6 and 24h (vorinostat)
  • organism-icon Homo sapiens
  • sample-icon 526 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Human Genome U133A Array (hthgu133a), Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

To identify patterns of drug-induced gene modulation that occur across different cell types, we measured gene expression changes across NCI-60 cell lines after exposure to 15 anticancer agents. The results were integrated into a database and set of interactive analysis tools, the NCI Transcriptional Pharmacodynamics Workbench (NCI TPW), intended to allow exploration of gene expression modulation, including by molecular pathway, drug target, and association with drug sensitivity. We identified common transcriptional responses across drugs and cell types and uncovered cell signaling pathwayspecific gene expression changes associated with drug sensitivity. We also demonstrated the value of this tool for investigating clinically relevant molecular hypotheses, utilizing the NCI TPW to assess drug-induced expression changes in genes associated with immune function and epithelial-mesenchymal transition, and to identify candidate biomarkers for drug activity. The NCI TPW provides a comprehensive resource to facilitate understanding of tumor cell characteristics that define sensitivity to anticancer drugs.

Publication Title

The NCI Transcriptional Pharmacodynamics Workbench: A Tool to Examine Dynamic Expression Profiling of Therapeutic Response in the NCI-60 Cell Line Panel.

Sample Metadata Fields

Specimen part

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)

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Developed by the Childhood Cancer Data Lab

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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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