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accession-icon SRP064484
Allelic Series of Huntington''s Disease Knock-in Mice Reveals Expression Discorrelates
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We report a simultaneous comparison of striatal mRNA levels by RNA sequencing mice with graded levels of HD-like abnormalities Overall design: Examination of 4 different mouse lines

Publication Title

Allelic series of Huntington's disease knock-in mice reveals expression discorrelates.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP076944
RNA-seq transcriptome analysis of epidermal CD8+CD103+CD49a+ and CD8+CD103+CD49- T cells from healthy human skin
  • organism-icon Homo sapiens
  • sample-icon 53 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We report the transcriptome analysis of epidermal CD8 tissue resident memory T (TRM) cells from healthy human skin. Specifically, epidermal CD8+CD103+CD49a+ and CD8+CD103+CD49- TRM cells from healthy human skin were sorted by FACS. Differential gene expression analysis revealed functional dichotomy of epidermal CD8+CD103+CD49a+ and CD8+CD103+CD49- TRM cells. Overall design: Analysis of differentially expressed genes between epidermal CD8+CD103+CD49a+ and CD8+CD103+CD49- T cells from healthy human skin, biological replicates (n=7) (healthy skin donors).

Publication Title

CD49a Expression Defines Tissue-Resident CD8<sup>+</sup> T Cells Poised for Cytotoxic Function in Human Skin.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE90864
Microarray analysis of innate immune response induced by immunization with the adjuvant QS-21 in lymph node and muscle in mice.
  • organism-icon Mus musculus
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

The goal of this study was to identify the transcriptional mechanisms involved in the activation of the immune system by QS-21, a triterpene glycoside purified from the bark of Quillaja saponaria which has adjuvant activity in vivo. Saponins represent a promising class of vaccine adjuvant. Together with the TLR4-ligand MPL, QS-21 is part of the Adjuvant System AS01, a key component of the Malaria and Zoster candidate vaccines that display demonstrated clinical efficacy. However, the mechanism of action of QS-21 in this liposomal formulation is poorly understood. Upon intra-muscular immunisation, we observed that QS-21 rapidly accumulated in CD169+ resident macrophages of the draining lymph node where it elicited a local innate immune response. Depletion of these cells abrogated QS-21-mediated innate cell recruitment to the lymph node, dendritic cell (DC) phenotypic maturation as well as the adjuvant effect on T cell and antibody responses to co-administered antigens. DCs rather than lymph node-resident macrophages were directly involved in T cell priming by QS-21 as revealed by the decrease in antigen-specific T cell response in Batf3/ mice. Further analysis showed that the adjuvant effect of QS-21 depended on the integration of Caspase-1 and MyD88 pathways, at least in part through the local release of HMGB1. Taken together, this work unravels the key role of lymph node sentinel macrophage in controlling the adjuvant effect of a molecule proven to improve vaccine response in humans

Publication Title

Central Role of CD169&lt;sup&gt;+&lt;/sup&gt; Lymph Node Resident Macrophages in the Adjuvanticity of the QS-21 Component of AS01.

Sample Metadata Fields

Specimen part

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accession-icon E-MEXP-122
Transcription profiling of leukemic cells of monozygotic twins
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

We established gene expression profiles of diagnostic bone marrow samples of monozygotic twins with acute lymphoblastic leukemia. We established technical duplicates for each twin.

Publication Title

Prenatal origin of separate evolution of leukemia in identical twins.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage

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accession-icon SRP039511
Fed State Prior to Hemorrhagic Shock and Polytrauma in a Porcine Model Results in Altered Liver Transcriptomic Response
  • organism-icon Sus scrofa
  • sample-icon 90 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We sequenced liver mRNA from 23 individual pigs (5 prefed and 18 fasted) taken at 4 separate time points to evaluate the change in gene expression over the course of hemorrhagic shock and resuscitation in response to a carbohydrate prefed state. Overall design: Examination of mRNA levels in liver biopsies from pigs at 4 timepoints throughout hemorrhagic shock and resuscitation

Publication Title

Fed state prior to hemorrhagic shock and polytrauma in a porcine model results in altered liver transcriptomic response.

Sample Metadata Fields

Specimen part, Cell line, Subject, Time

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accession-icon GSE22337
UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is an inducer of apoptotic processes in Capan-1 pancreatic carcinoma cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Loss of UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase (GNE) induces apoptotic processes in pancreatic carcinoma cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE22334
Induction of apoptotic processes in Capan-1 pancreatic carcinoma cells by restoration of p16INK4a expression
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Early invasive growth and metastasis are features of pancreatic cancer that rely on resistance to anoikis, an apoptosis program activated upon loss of adequate matrix anchorage. Re-expression of the tumor suppressor p16 reversed anoikis resistance of pancreatic cancer cells. This conversion to an anoikis-susceptible phenotype was found to be associated with a striking loss of GNE mRNA expression, prompting us to address the role of GNE in pancreatic cancer in more detail. GNE catalyzes a rate-limiting key step of the sialic acid biosynthesis and may have additional functions in the nucleus.

Publication Title

Loss of UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase (GNE) induces apoptotic processes in pancreatic carcinoma cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE22336
UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is an inducer of apoptotic processes in Capan-1 pancreatic carcinoma cells: GNE silencing
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Early invasive growth and metastasis are features of pancreatic cancer that rely on resistance to anoikis, an apoptosis program activated upon loss of adequate matrix anchorage. Re-expression of the tumor suppressor p16 reversed anoikis resistance of pancreatic cancer cells. This conversion to an anoikis-susceptible phenotype was found to be associated with a striking loss of GNE mRNA expression, prompting us to address the role of GNE in pancreatic cancer in more detail. GNE catalyzes a rate-limiting key step of the sialic acid biosynthesis and may have additional functions in the nucleus.

Publication Title

Loss of UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase (GNE) induces apoptotic processes in pancreatic carcinoma cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE60542
Revisiting the transcriptional analysis of primary tumors and associated nodal metastases with enhanced biological and statistical controls: application to thyroid cancer
  • organism-icon Homo sapiens
  • sample-icon 88 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The biology underlying nodal metastasis is poorly understood. Transcriptome profiling has helped to characterize both primary tumors seeding nodal metastasis and the metastasis themselves. The interpretation of these data, however, is not without ambiguities. Here we profiled the transcriptomes of 17 papillary thyroid cancer (PTC) nodal metastases, associated primary tumors and primary tumors from N0 patients. We also included patient-matched normal thyroid and lymph node samples as controls to address some limits of previous studies. We found that the transcriptomes of patient-matched primary tumors and metastases were more similar than of unrelated metastases/primary pairs, a result also reported in other organ systems, and that part of this similarity reflected patient background. We found that the comparison of patient-matched primary tumors and metastases was heavily confounded by the presence of lymphoid tissues in the metastasis samples. An original data adjustment procedure was developed to circumvent this problem. It revealed a differential expression of stroma-related gene expression signatures also regulated in other organ systems. The comparison of N0 vs. N+ primary tumors uncovered a signal irreproducible across independent PTC datasets. This signal was also detectable when comparing the normal thyroid tissues adjacent to N0 and N+ tumors, suggesting a cohort specific bias also likely to be present in previous studies with similar statistical power. Classification of N0 vs. N+ yielded an accuracy of 63%, but additional statistical controls not presented in previous studies, revealed that this is likely to occur by chance alone. To address this issue, we used large datasets from The Cancer Genome Atlas and showed that N0 vs. N+ classification rates could not be reached randomly for most cancers. Yet, it was significant, but of limited accuracy (<70%) for thyroid, breast and head and neck cancers.

Publication Title

Revisiting the transcriptional analysis of primary tumours and associated nodal metastases with enhanced biological and statistical controls: application to thyroid cancer.

Sample Metadata Fields

Sex

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accession-icon GSE8171
Prox-1 promotes invasion of kaposiform hemangioendotheliomas
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Kaposis sarcoma (KS) is the most frequently occurring malignant tumor in patients infected with the human immunodeficiency virus. Recent studies have revealed that infection of vascular endothelial cells with Kaposi's sarcoma-associated herpes virus in vitro results in a lymphatic re-programming of these cells, with potent induction of the lymphatic marker genes podoplanin and VEGFR-3 which is mediated by upregulation of the transcription factor Prox1. However, the potential effects of Prox1 expression on the biology of KS and, in particular, on the aggressive and invasive behavior of KS tumors in vivo have remained unknown. We stably expressed Prox1 cDNA in the two mouse hemangioendothelioma cell lines EOMA and Py-4-1, well-established murine models for kaposiform hemangioendothelioma. Surprisingly, we found that expression of Prox1 was sufficient to induce a more aggressive behavior of tumors growing in syngenic mice, leading to enhanced local invasion into the muscular layer and to cellular anaplasia. This enhanced malignant phenotype was associated with upregulation of several genes involved in proteolysis, cytoskeletal reorganisation and migration. Together, these results indicate that Prox1 plays an important, previously unanticipated role in mediating the aggressive behavior of vascular neoplasms such as Kaposi's sarcoma.

Publication Title

Prox-1 promotes invasion of kaposiform hemangioendotheliomas.

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)

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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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