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accession-icon GSE15852
Expression data from human breast tumors and their paired normal tissues
  • organism-icon Homo sapiens
  • sample-icon 86 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Microarray is widely used to monitor gene expression changes in breast cancer. The transcriptomic changes in breast cancer is commonly occured during the transition of normal cells to cancerous cells. This is the first study on gene expression profiling of multi ethnic of Malaysian breast cancer patients (Malays, Chinese and Indian). We aim to identify differentially expressed genes between tumors and normal tissues. We have identified a set of 33 significant differentially expressed genes in the tumor vs. normal group at p<0.001.

Publication Title

Gene expression patterns distinguish breast carcinomas from normal breast tissues: the Malaysian context.

Sample Metadata Fields

Specimen part, Disease stage, Race

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accession-icon GSE54775
Effect of choline kinase inhibitor hexadecyltrimethylammonium bromide on Plasmodium falciparum gene expression
  • organism-icon Plasmodium falciparum
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Plasmodium/Anopheles Genome Array (plasmodiumanopheles)

Description

Investigations on the fundamental of malaria parasite biology, such as invasion, growth cycle, metabolism and cell signalling have uncovered a number of potential antimalarial drug targets, including choline kinase, a key enzyme involved in the synthesis of phosphatidylcholine, an important component in parasite membrane compartment.

Publication Title

Effect of choline kinase inhibitor hexadecyltrimethylammonium bromide on Plasmodium falciparum gene expression.

Sample Metadata Fields

Treatment

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accession-icon SRP056103
Diabetes Enhances the Proliferation of Adult Pancreatic Multipotent Progenitor Cells and Biases Their Differentiation to More Beta-Cell Production
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Endogenous pancreatic multipotent progenitors (PMPs) are ideal candidates for regenerative approaches to compensate for b-cell loss since their b-cell–producing capacities as well as strategic location would eliminate unnecessary invasive manipulations. However, little is known about the status and potentials of PMPs under diabetic conditions. Here we show that b-cell metabolic stress and hyperglycemia enhance the proliferation capacities of adult PMP cells and bias their production of progeny toward b-cells in mouse and human. These effects are dynamic and correlate with functional b-cell regeneration when conditions allow. Overall design: Insulin-positive Glut2-low cell population of adult pancreatic tissue is enriched for PMP cells. Streptozocin (STZ) can enter beta-cells via Glut2 , induce cell death and consequently diabetes. Insulin-positive cells from two groups (STZ-injected experiment and vehicle-injected control, n=3/group) of MIP-GFP transgenic male mice were sorted to Glut2-low (Glut2L) and Glut2-high (Glut2H) by FACS. Total RNA from these samples were extracted for transcriptome analysis.

Publication Title

Diabetes enhances the proliferation of adult pancreatic multipotent progenitor cells and biases their differentiation to more β-cell production.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP045579
Genome-wide mapping of promoter-enhancer interactions with HiCap [RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina Genome Analyzer II

Description

Although the locations of promoters and enhancers have been identified in several cell types, we have yet limited information on their connectivity. We developed HiCap, which combines Hi-C with promoter sequence capture, to enable genome-wide identification of regulatory interactions with single-enhancer resolution. HiCap analyses of mouse embryonic stem cells (mESC) identified promoter-enhancer interactions predictive of gene expression change upon perturbation, opening up for genomic analyses of long-range gene regulation. Overall design: HiCap was designed by combining Hi-C with with sequence capture (for all promoters) and carried out in mouse embryonic stem cells (mESC)

Publication Title

Genome-wide mapping of promoter-anchored interactions with close to single-enhancer resolution.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE9946
Comparison of stimulatory and inhibitory dendritic cell subsets reveals new role of DC in granulomatous infection
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Myeloid dendritic cells (DC) and macrophages play an important role in pathogen sensing and antimicrobial defense. Recently we demonstrated that infection of human DC with intracellular bacterium Listeria monocytogenes (L.monocytogenes) leads to the induction of the immunoinhibitory enzyme indoleamine 2,3-dioxygenase (Popov et al., J Clin Invest, 2006), while in the previous studies L.monocytogenes infection was associated with a rather stimulatory DC phenotype. To clarify this discrepancy we performed comparative microarray analysis of immature mo-DC (immDC), mature stimulatory mo-DC (matDC) and mature inhibitory DC either stimulated with prostaglandin E2 (PGE2-DC) or infected with L.monocytogenes (infDC). Studying infection of human myeloid DC with Listeria monocytogenes, we found out, that infected DC are modified by the pathogen to express multiple inhibitory molecules, including indoleamine 2,3-dioxygenase (IDO), cyclooxygenase-2, interleukin 10 and CD25, which acts on DC as IL-2 scavenger. All these inhibitory molecules, expressed on regulatory DC (DCreg), are strictly TNF-dependent and are in concert suppressing T-cell responses. Moreover, only DCreg can efficiently control the number of intracellular listeria, mostly by IDO-mediated mechanisms and by other factors, remaining to be identified. Analyzing publicly acessible data of transcriptional changes in DC and macrophages, infected by various pathogens and parasites (GEO, GSE360), we noticed that infection of these cells with Mycobacterium tuberculosis causes transcriptional response, comparable with the one caused by listeria in human DC. In fact, granuloma in tuberculosis and listeriosis in vivo are enriched for myeloid DC and macrophages characterized by regulatory phenotype.

Publication Title

Infection of myeloid dendritic cells with Listeria monocytogenes leads to the suppression of T cell function by multiple inhibitory mechanisms.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE73125
Transcriptome-based profiling reveals a macrophage pedigree and identifies Irf8 as pivotal for macrophage homeostasis and function
  • organism-icon Mus musculus
  • sample-icon 81 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

Recent studies have shown that tissue macrophages (MF) arise from embryonic progenitors of the yolk sac (YS) and fetal liver and colonize the tissues before birth. Further studies have proposed that developmentally distinct tissue MF can be identified based on the differential expression of F4/80 and CD11b, but whether a characteristic transcriptional profile exists is largely unknown. Here, we established an inducible fate mapping system that facilitated the identification of A2 progenitors of the YS as source of F4/80hi but not CD11bhi MF. Large-scale transcriptional profiling of MF precursors from the YS until adulthood allowed the description of a complex MF pedigree. We further identified a distinct molecular signature of F4/80hi and CD11bhi MF and found that Irf8 was vital for MF maturation and the innate immune response. Our data provide new cellular and molecular insights into the origin and developmental pathways of tissue MF.

Publication Title

Transcriptome-based profiling of yolk sac-derived macrophages reveals a role for Irf8 in macrophage maturation.

Sample Metadata Fields

Specimen part

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accession-icon SRP102683
Transcriptional responses induced by controlled human malaria infection (CHMI)
  • organism-icon Homo sapiens
  • sample-icon 39 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Whole blood RNA-Seq was applied to investigate gene expression kinetics in Tanzanian males who underwent controlled malaria infection by intradermal injection with aseptic, purified, cryopreserved Plasmodium falciparum sporozoites. Overall design: 10 volunteers injected intradermally with a total of 25'000 infectious Plasmodium falciparum sporozoites (PfSPZ).

Publication Title

Whole blood transcriptome changes following controlled human malaria infection in malaria pre-exposed volunteers correlate with parasite prepatent period.

Sample Metadata Fields

Subject

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accession-icon SRP049669
CX3CR1/Fractalkine receptor expression separates memory CD8+ T cells with distinct functional profiles (RNA-seq)
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq1000

Description

Memory T cells are important for protective immunity against infectious microorganisms. Such protection is achieved by cooperative action of memory T cell populations that differ in their tissue localization and functionality. We report on the identification of the fractalkine receptor CX3CR1 as marker for stratification of memory T cells with cytotoxic effector function from those with proliferative function in both, mice and man. Based on CX3CR1 and CD62L expression levels four distinct memory T cell populations can be distinguished based on their functional properties. Transcriptome and proteome profiling revealed that CX3CR1 expression was superior to CD62L to resolve memory T cell functionality and allowed determination of a core signature of memory T cells with cytotoxic effector function. This identifies a CD62Lhi CX3CR1+ memory T cell population with an identical gene signature to CD62LlowCX3CR1+ effector memory T cells. In lymph nodes, this so far unrecognized CD62LhiCX3CR1+ T cell population shows a distinct migration pattern and anatomic positioning compared to CD62LhiCX3CR1neg TCM. Furthermore, CX3CR1+ memory T cells were scarce or absent during chronic HBV, HCV and HIV infection in man and chronic LCMV infection in mice confirming the value of CX3CR1+ in understanding principles of protective immune memory. Overall design: CD8+ T cells were isolated and directly assessed. After harvesting, cells were immediately lysed in Trizol (Invitrogen) before storage at -80°C for RNA isolation.

Publication Title

Functional classification of memory CD8(+) T cells by CX3CR1 expression.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE40352
The effects of NAC on gene expression in Nkx3.1-/- mouse prostate
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We tested the effects of the antioxidant NAC (N-Acetyl-Cysteine) on gene expression in Nkx3.1-deficient mouse prostate.

Publication Title

Antioxidant treatment promotes prostate epithelial proliferation in Nkx3.1 mutant mice.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE57194
In Vitro Transformation of Primary Human CD34+ Cells by AML Fusion Oncogenes: Early Gene Expression Profiling Reveals Possible Drug Target in AML
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Different fusion oncogenes in acute myeloid leukemia (AML) have distinct clinical and laboratory features suggesting different modes of malignant transformation. Here we compare the in vitro effects of representatives of major groups of AML fusion oncogenes on primary human CD34+ cells.

Publication Title

In vitro transformation of primary human CD34+ cells by AML fusion oncogenes: early gene expression profiling reveals possible drug target in AML.

Sample Metadata Fields

Specimen part

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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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