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accession-icon GSE7831
Expression data from immature pDC and pDC activated with CpG 1826 and influenza virus PR8
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

CpG 1826 binds to Toll-like receptor (TLR)9, whereas influenza virus PR8 activates pDC via TLR7. Differential stimulation of pDCs is expected to result in unique activation mechanism(s) leading to a different phenotypically and functionally matured pDC

Publication Title

Two distinct activation states of plasmacytoid dendritic cells induced by influenza virus and CpG 1826 oligonucleotide.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE58721
BRAF inhibition leads to oxidative phosphorylation and cellular senescence in human melanoma cells
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Targeting components of the mitogen-activated protein kinase (MAPK) pathway prolongs survival of patients with advanced BRAFV600E melanomas but such an approach is not curative because of the rapid acquisition of numerous resistance mechanisms. Here we analyze melanoma cells that evade MAPK inhibitors by undergoing a senescence-like, slow-growth, phenotype, which leads to acquired resistance. The initial therapeutic response is characterized by an integrated stress response program, including stimulation of autophagic flux, activation of the endoplasmic reticulum machinery, and an enhanced ability of detoxifying reactive oxygen species. Reversibly senescent cells also exhibit an increase in mitochondrial genome copy number and a strong metabolic shift towards oxidative phosphorylation (OxPhos). Inducing mitochondrial dysfunction by co-targeting the MAPK pathway and mitochondrial Hsp90-directed protein folding with specific inhibitors prevented entry of cells into a reversibly senescent state, suppressed mitochondrial energy metabolism and augmented therapy response.

Publication Title

Targeting mitochondrial biogenesis to overcome drug resistance to MAPK inhibitors.

Sample Metadata Fields

Disease, Disease stage, Cell line, Time

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accession-icon GSE69834
Bone marrow neutrophils regulate multiple myeloma by releasing DNA
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Development of Multiple Myeloma is associated with an accumulation of myeloid derived suppressor cells (MDSCs ) - cells that are morphologically and phenotypically similar to neutrophils (PMN-MDSC) and monocytes (M-MDSC), but are distinct in their functional and biochemical characteristics as well as in their ability to suppress immune responses.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE50436
Gene expression data from murine mDC and pDC
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

mDC and pDC exhibit distinct TLR expression pattern and differ in their responses to various TLR ligands. The goal of this study was to identify genes, that were differentally expressed between mDC and pDC as a means to determine how TLR signaling pathways operate. Suprisingly, expression of TLR-assoociated signaling proteins were found to be present at equivalent levels between mDC and pDC, despite differential expression of TLRs, and thus revealing insight into use of adaptor proteins that function as general regulators of TLR signaling pathways in both cell types.

Publication Title

A promiscuous lipid-binding protein diversifies the subcellular sites of toll-like receptor signal transduction.

Sample Metadata Fields

Specimen part

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accession-icon GSE13255
Gene Expression Profiles in Peripheral Blood Mononuclear Cells Can Distinguish Patients with NonSmall Cell Lung Cancer.
  • organism-icon Homo sapiens
  • sample-icon 291 Downloadable Samples
  • Technology Badge IconIllumina human-6 v2.0 expression beadchip

Description

We report a 29-gene diagnostic signature, which distinguishes individuals with NSCLC from controls with non-malignant lung disease with 91% Sensitivity, 79% Specificity and a ROC AUC of 92%. Accuracy on an independent set of 18 NSCLC samples from the same location was 79%. Samples from an independent location including 12 stage 1 NSCLC and 15 controls, achieved an accuracy of 74%. A study of 18 paired samples taken pre and post surgery shows that the PBMC associated cancer signature is significantly reduced after tumor removal, supporting the hypothesis that the signature detected in pre-surgery samples is a response to the presence of the tumor.

Publication Title

Gene expression profiles in peripheral blood mononuclear cells can distinguish patients with non-small cell lung cancer from patients with nonmalignant lung disease.

Sample Metadata Fields

Sex, Age, Race

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accession-icon GSE92765
LPAR signaling activated in neural crest stem cells promotes melanoma cell growth, invasion and therapy resistance
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip, Illumina HumanWG6_V2 chip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE45405
Examination of the MAPK pathway gene expression in patient samples
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge IconIllumina humanRef-8 v2.0 expression beadchip

Description

Microarray analysis of total RNA isolated from samples of circulating tumor cells from 7 patients before romidepsin infusion (0 hours), at 4 h after initiation of the infusion (4 hours) and 24 h after initiation of the infusion (24 hours).

Publication Title

MAPK pathway activation leads to Bim loss and histone deacetylase inhibitor resistance: rationale to combine romidepsin with an MEK inhibitor.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE37614
Human breast cancer associated fibroblasts exhibit subtype specific gene expression profiles
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Breast cancer is a heterogeneous disease for which prognosis and treatment strategies are largely governed by the receptor status (estrogen, progesterone and Her2-neu) of the tumor cells. Gene expression profiling of whole breast tumors further stratifies breast cancer into several molecular subtypes which also co-segregate with the receptor status of the tumor cells. We postulated that cancer associated fibroblasts (CAFs) within the tumor stroma may exhibit subtype specific gene expression profiles and thus contribute to the biology of the disease in a subtype specific manner. Several studies have reported gene expression profile differences between CAFs and normal breast fibroblasts but in none of these studies were the results stratified based on tumor subtypes. To address whether gene expression in breast cancer associated fibroblasts varies between breast cancer subtypes, we compared the gene expression profiles of early passage primary CAFs isolated from twenty human breast cancer samples representing three main subtypes; seven ER+, seven triple negative (TNBC) and six Her2+. We observed significant expression differences between CAFs derived from Her2+ breast cancer and CAFs from TNBC and ER+ cancers, particularly in pathways associated with cytoskeleton and integrin signaling. In the case of Her2+ breast cancer, the signaling pathways found to be selectively up regulated in CAFs may contribute to the more invasive properties and unfavorable prognosis of Her2+ breast cancer. These data demonstrate that in addition to the distinct molecular profiles that characterize the neoplastic cells, CAF gene expression is also differentially regulated in distinct subtypes of breast cancer.

Publication Title

Human breast cancer associated fibroblasts exhibit subtype specific gene expression profiles.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE43254
Transcriptomic Analysis Comparing Tumor-Associated Neutrophils with Granulocytic Myeloid-Derived Suppressor Cells and Normal Neutrophils
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

The role of myeloid cells in supporting cancer growth is well established. Most work has focused on myeloid-derived suppressor cells (MDSC) that accumulate in tumor-bearing animals, but tumor-associated neutrophils (TAN) are also known to be capable of augmenting tumor growth. However, little is known about their evolution, phenotype, and relationship to naive neutrophils (NN) and to the granulocytic fraction of MDSC (G-MDSC). In the current study, a transcriptomics approach was used in mice to compare these cell types. Our data show that the three populations of neutrophils are significantly different in their mRNA profiles with NN and G-MDSC being more closely related to each other than to TAN. Structural genes and genes related to cell-cytotoxicity (i.e. respiratory burst) were significantly down-regulated in TAN. In contrast, many immune-related genes and pathways, including genes related to the antigen presenting complex (e.g. all six MHC-II complex genes), and cytokines (e.g. TNF-a, IL-1-a/b), were up-regulated in G-MDSC, and further up-regulated in TAN. Thirteen of the 25 chemokines tested were markedly up-regulated in TAN compared to NN, including striking up-regulation of chemoattractants for T/B-cells, neutrophils and macrophages. This study characterizes different populations of neutrophils related to cancer, pointing out the major differences between TAN and the other neutrophil populations.

Publication Title

Transcriptomic analysis comparing tumor-associated neutrophils with granulocytic myeloid-derived suppressor cells and normal neutrophils.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE20613
The Sp100 component of ND10/PML bodies is a potent tumor suppressor
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina human-6 v2.0 expression beadchip

Description

Identifying the functions of proteins, which define specific subnuclear structures and territories, is important for understanding eukaryotic nuclear dynamics. Sp100 is a prototypical protein of ND10/PML bodies and co-localizes with the proto-oncogenic protein PML and Daxx, proteins with critical roles in oncogenic transformation, interferon-mediated viral resistance and response to PML-directed cancer therapeutics. Sp100 isoforms contain PHD, Bromo and HMG domains and are highly sumoylated at ND10/PML bodies, all characteristics suggestive of a role in chromatin mediated gene regulation. However, no clear role for the Sp100 component of PML bodies in oncogenesis has been defined. Using isoform-specific knockdown techniques, we show that most human diploid fibroblasts, which lack Sp100, rapidly senesce and discuss gene expression changes associated with this rapid senescence.

Publication Title

Sp100 as a potent tumor suppressor: accelerated senescence and rapid malignant transformation of human fibroblasts through modulation of an embryonic stem cell program.

Sample Metadata Fields

Cell line, Treatment

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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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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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