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accession-icon GSE11386
Gene expression in murine memory versus naive B cells (1st generation and 2nd generation screens)
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Memory B cells play essential roles in the maintenance of long-term immunity and may be important in the pathogenesis of autoimmune disease, but how these cells are distinguished from their nave precursors is poorly understood. To address this, it would be important to understand how gene expression differs between memory and naive B cells in order to elucidate memory-specific functions. Using model systems that help overcome the lack of murine memory-specific markers and the low frequency of antigen-specific memory and nave cells, we undertook a global comparison of gene expression between memory B cells and their naive precursors.

Publication Title

Systematic comparison of gene expression between murine memory and naive B cells demonstrates that memory B cells have unique signaling capabilities.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE51604
Memory B cell subset defined by CD80 and PD-L2 surface expression
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

NP-reactive murine splenic memory B cells were sorted based on the expression of the surface markers CD80 and PD-L2

Publication Title

CD80 and PD-L2 define functionally distinct memory B cell subsets that are independent of antibody isotype.

Sample Metadata Fields

Specimen part

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accession-icon GSE17891
Pervasive subtypes of pancreatic ductal adenocarcinoma (PDA) and their differing response to therapy.
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 61 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Pancreatic ductal adenocarcinoma (PDA) carries a dismal prognosis and current treatments are only modestly effective. We present evidence that this variation is caused in part by recurrent, pervasive molecular differences between tumors. mRNA expression profiles measured using microdissected PDA clinical samples reveal three dominant subtypes of disease; epithelial, mesenchymal and acinar-like. The classical and quasi-mesenchymal subtypes are observed in human and mouse PDA cell lines. Importantly, responses to cytotoxics and KRAS depletion in human PDA cell lines differ substantially between subtypes, and in opposing directions. Integrated genomics implicate and functional studies support overexpression of the trancription factor GATA6 as a driver of the epithelial subtype. These results provide a molecular framework for evaluating the prospects of personalized treatment in PDA.

Publication Title

Subtypes of pancreatic ductal adenocarcinoma and their differing responses to therapy.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP157936
Transcriptomic analysis of T84 colon carcinoma cell line treated with trametinib, JQ1 or their combination
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

T84 cells were treated with DMSO, 30nM trametinib (MEKi), 1µM JQ1 (BRD4i) or the combination of trametinib and JQ1 (combo) for 24h. Overall design: 3 replicates per condition were analyzed by RNA-seq.

Publication Title

Suppression of interferon gene expression overcomes resistance to MEK inhibition in KRAS-mutant colorectal cancer.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon SRP157753
Transcriptomic analysis of trametinib-resistant HCT116 colorectal carcinoma cells compared to the parental control cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

HCT116 cells were treated with with increasing concentrations of trametinib over 2 months. Drug-resistant clones emerged and were cultured in the presence of 30 nmol/L trametinib. These cells exhibited a greater than 10-fold increase in the GI50 for trametinib compared to the parental cell line. RNA-seq of the resistant clone HCT116_R4 versus the parental cells identified differentially expressed genes potentially involved in resistance. Overall design: For the parental and resistant clone, 3 replicates each were analysed by RNA-seq.

Publication Title

Suppression of interferon gene expression overcomes resistance to MEK inhibition in KRAS-mutant colorectal cancer.

Sample Metadata Fields

Treatment, Subject

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accession-icon GSE53169
Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer
  • organism-icon Mus musculus
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE53167
Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer (part 1)
  • organism-icon Mus musculus
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Activating mutations in KRAS are among the most frequent events in diverse human carcinomas and are particularly prominent in human pancreatic ductal adenocarcinoma (PDAC). An inducible KrasG12D-driven mouse model of PDAC has established a critical role for sustained KrasG12D expression in tumor maintenance, providing a model to determine the potential for, and underlying mechanisms of, KrasG12Dindependent PDAC recurrence. Here we show that some tumors undergo spontaneous relapse and are devoid of KrasG12D expression and downstream canonical MAPK signaling and instead acquired amplification and overexpression of the transcriptional co-activator Yap1. Functional studies established the role of Yap1 and the transcriptional factor Tead2 in driving KrasG12Dindependent tumor maintenance. The Yap1/Tead2 complex acts cooperatively with E2F transcription factors to activate a cell cycle and DNA replication program. Our studies, along with corroborating evidence from human PDAC models, portend a novel mechanism of escape from oncogenic Kras addiction in PDAC.

Publication Title

Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE53168
Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer (part 2)
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Activating mutations in KRAS are among the most frequent events in diverse human carcinomas and are particularly prominent in human pancreatic ductal adenocarcinoma (PDAC). An inducible KrasG12D-driven mouse model of PDAC has established a critical role for sustained KrasG12D expression in tumor maintenance, providing a model to determine the potential for, and underlying mechanisms of, KrasG12Dindependent PDAC recurrence. Here we show that some tumors undergo spontaneous relapse and are devoid of KrasG12D expression and downstream canonical MAPK signaling and instead acquired amplification and overexpression of the transcriptional co-activator Yap1. Functional studies established the role of Yap1 and the transcriptional factor Tead2 in driving KrasG12Dindependent tumor maintenance. The Yap1/Tead2 complex acts cooperatively with E2F transcription factors to activate a cell cycle and DNA replication program. Our studies, along with corroborating evidence from human PDAC models, portend a novel mechanism of escape from oncogenic Kras addiction in PDAC.

Publication Title

Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE27031
The MuvB complex sequentially recruits B-Myb and FoxM1 to promote mitotic gene expression
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The MuvB complex sequentially recruits B-Myb and FoxM1 to promote mitotic gene expression.

Sample Metadata Fields

Cell line

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accession-icon SRP127325
Patient-derived organoids (PDOs) model treatment response of metastatic gastrointestinal cancers.
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

We report RNAseq data from subsequent passages of five organoid cultures. Overall design: RNA extracted from subsequent PDO passages was subjected to RNAseq.

Publication Title

Patient-derived organoids model treatment response of metastatic gastrointestinal cancers.

Sample Metadata Fields

Disease, Subject

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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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