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accession-icon SRP173228
Single-cell RNA-seq of UTCaß population in sarcoma mice models
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Neutrophils represent a fundamental mechanism of antimicrobial resistance and inflammation 1. Moreover, neutrophils have emerged as important players in the activation, orchestration and regulation of adaptive immune responses2,3. Neutrophils are a component of the tumor microenvironment (TME) and have been prevalently shown to promote progression 4-6. On the other hand, unleashed neutrophilic effectors have also been reported to mediate anti-cancer resistance7-11. Antibody-mediated depletion used to investigate the role of neutrophils in tumor progression suffers from limitations, including duration, specificity and perturbation of the system12. We therefore used a genetic approach to investigate the role of neutrophils in primary 3-methylcholanthrene (3-MCA)-induced sarcomagenesis. Neutrophils were found to play an essential role in resistance against primary carcinogenesis by driving an interferon-? dependent type 1 immune response. Neutrophil-dependent macrophage production of IL-12p70 led to type 1 polarization of CD4- CD8- unconventional aß T cells (UTCaß) in the TME. Single cell RNAseq analysis and in vivo evidence from two preclinical sarcoma models highlight the antitumor potential of a UTCaß subset. In the TCGA cohort of human undifferentiated pleomorphic sarcomas (UPS), unlike other sarcomas, granulocyte-colony stimulating factor receptor (CSF3R) expression and a neutrophil signature were associated with better outcome and with a type 1 immune response. The positive association between high neutrophil infiltration and improved clinical outcome was confirmed in an independent UPS cohort by immunohistochemistry. Thus, neutrophils, by driving a type 1 immune response and polarization of UTCaß, mediate resistance against murine and human sarcomas. Overall design: two experimental conditions, two biological replicates for each condition

Publication Title

Neutrophils Driving Unconventional T Cells Mediate Resistance against Murine Sarcomas and Selected Human Tumors.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE77173
Gene expression profiling of Mec-1 cells upon chronic silencing of HIF-1a
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

This experiment was carried out in the context of a study aimed to identify the function of the transcription facotrs HIF-1a in the pathogenesis of chronic lymphocytic leukemia (CLL).

Publication Title

HIF-1α regulates the interaction of chronic lymphocytic leukemia cells with the tumor microenvironment.

Sample Metadata Fields

Sex, Cell line

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accession-icon GSE42495
Macrophages in T cell/histiocyte rich B cell lymphoma strongly express metal-binding proteins and show a bi-activated phenotype
  • organism-icon Homo sapiens
  • sample-icon 47 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

In a supervised principal component analysis, histiocytes from TCHRBCL were most closely related to epithelioid cells from NLPHL, with both types of cells expressing genes related to proinflammatory and regulatory macrophage activity.

Publication Title

Macrophages in T cell/histiocyte rich large B cell lymphoma strongly express metal-binding proteins and show a bi-activated phenotype.

Sample Metadata Fields

Specimen part

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accession-icon GSE76757
Combination of the MEK inhibitor pimasertib with BTK or PI3K-delta inhibitors is active in pre-clinical models of aggressive lymphomas
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

assess the efficacy of Pimasertib to characterize its mechanism of action

Publication Title

Combination of the MEK inhibitor pimasertib with BTK or PI3K-delta inhibitors is active in preclinical models of aggressive lymphomas.

Sample Metadata Fields

Cell line, Treatment, Time

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accession-icon GSE32112
Gene expression data from muscle sample of pig commercial herd Pix(DLxDE).
  • organism-icon Sus scrofa
  • sample-icon 206 Downloadable Samples
  • Technology Badge Icon Affymetrix Porcine Genome Array (porcine)

Description

In this study, we used correlation analysis of the expression profiles and carcass traits to produce a list of functional candidate genes under the assumption that genes with strong correlation between their expression values and drip belong to pathways or networks relevant for the control of the trait.

Publication Title

Elucidating molecular networks that either affect or respond to plasma cortisol concentration in target tissues of liver and muscle.

Sample Metadata Fields

Specimen part

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accession-icon GSE29340
Microarray analysis reveals genes and functional networks relevant to the predisposition for inverted teats in pigs
  • organism-icon Sus scrofa
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Porcine Genome Array (porcine)

Description

The inverted teat defect is an inherited disorder characterised by the failure of teats to protrude from the udder surface. The number and identity of relevant genes are unknown.

Publication Title

Microarray analysis reveals genes and functional networks relevant to the predisposition to inverted teats in pigs.

Sample Metadata Fields

Specimen part

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accession-icon GSE32956
Global transcriptome analysis of mammary tissue during fetal bud formation and growth in two pig breeds
  • organism-icon Sus scrofa
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Porcine Genome Array (porcine)

Description

The mammary gland development in swine begins at embryogenesis. The number and identity of relevant genes are unknown.

Publication Title

Gene expression analysis of mammary tissue during fetal bud formation and growth in two pig breeds--indications of prenatal initiation of postnatal phenotypic differences.

Sample Metadata Fields

Specimen part

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accession-icon GSE12195
Mutations of multiple genes deregulate the NF-kB pathway in diffuse large B cell lymphoma
  • organism-icon Homo sapiens
  • sample-icon 135 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Diffuse large B-cell lymphoma (DLBCL), the most common form of lymphoma in adulthood, comprises multiple biologically and clinically distinct subtypes including germinal center B cell-like (GCB) and activated B cell like (ABC) DLBCL. Gene expression profile studies have shown that its most aggressive subtype, ABC-DLBCL, is associated with constitutive activation of the NF-kB transcription complex. However, except for a small fraction of cases, it remains unclear whether NF-kB activation in these tumors represents an intrinsic program of the tumor cell of origin or a pathogenetic event. Here we show that >50% of ABC-DLBCL and a smaller fraction of GCB-DLBCL carry somatic mutations at multiple genes, including negative (TNFAIP3/A20) and positive (CARD11, TRAF2, TRAF5, MAP3K7/TAK1 and TNFRSF11A/RANK) regulators of NF-kB. Of these, the A20 gene, which encodes for a ubiquitin-modifying enzyme involved in termination of NF-kB responses, is the most commonly affected one, with ~30% of the patients displaying biallelic inactivation by mutations and/or deletions, suggesting a tumor suppressor role. Less frequently, missense mutations of TRAF2 and CARD11 produce molecules with significantly enhanced ability to activate NF-kB. Thus, our results demonstrate that NF-kB activation in DLBCL is caused by genetic lesions affecting multiple genes, whose loss or activation may promote lymphomagenesis by leading to abnormally prolonged NF-kB responses.

Publication Title

Mutations of multiple genes cause deregulation of NF-kappaB in diffuse large B-cell lymphoma.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE47044
Nodular lymphocyte predominant hodgkin lymphoma and T cell/histiocyte rich large B cell lymphoma - endpoints of a spectrum of one disease?
  • organism-icon Homo sapiens
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Tumor cells were microdissected from frozen sections of NLPHL and THRLBCL. RNA was amplified using the NUGEN WT-Ovation-One-direct-Kit. Samples were compared to tonsilar germinal center CD77 B cells.

Publication Title

Nodular lymphocyte predominant hodgkin lymphoma and T cell/histiocyte rich large B cell lymphoma--endpoints of a spectrum of one disease?

Sample Metadata Fields

Specimen part

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accession-icon GSE31312
Development and application of a new immunophenotypic algorithm for molecular subtype classification of Diffuse Large B-Cell Lymphoma (DLBCL): Report from an International DLBCL Rituximab-CHOP Consortium Program Study
  • organism-icon Homo sapiens
  • sample-icon 491 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We studied 498 de-novo adult DLBCL cases, which had been diagnosed between January 2002 and October 2009, as part of the International DLBCL Rituximab-CHOP Consortium Program Study

Publication Title

Addition of rituximab to chemotherapy overcomes the negative prognostic impact of cyclin E expression in diffuse large B-cell lymphoma.

Sample Metadata Fields

No sample metadata fields

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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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