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accession-icon GSE3059
Leukocytes Gene Expression in Correlation to Plasma Lipid Levels
  • organism-icon Homo sapiens
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Background---For decades, plasma lipid levels have been known risk factors of atherosclerosis. Recently, inflammation has gained acceptance as a crucial event in the pathogenesis and development of atherosclerosis. A number of studies have provided some insights into the relationships between the two aspects of atherosclerosis: plasma lipids --- the risk factors, and circulating leukocytes --- the effectors of inflammation. In this study, we investigate the relationships between plasma lipids and leukocytes.

Publication Title

Identifying leukocyte gene expression patterns associated with plasma lipid levels in human subjects.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE97689
Colorectal cancer initiation site
  • organism-icon Homo sapiens
  • sample-icon 92 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The role of stem cells in solid tumors remains controversial. In colorectal cancers (CRC), this is complicated by the conflicting top-down or bottom-up hypothesis of cancer initiation. We profiled the expressions of genes from the top (T) and bottom (B) fractions of the crypt in morphologically normal-appearing colonic mucosa (M) and contrasted this to that of matched mucosa adjacent to tumors (MT) in twenty three sporadic CRC patients. In thirteen patients, the genetic distance (M-MT) between the B fractions is smaller than the distance between the T fractions indicating that the expressions of significant genes diverge further in the top fractions (B<T). In the remaining ten patients, the reverse is observed (B>T).

Publication Title

Human colorectal cancer initiation is bidirectional, and cell growth, metabolic genes and transporter genes are early drivers of tumorigenesis.

Sample Metadata Fields

Specimen part

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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 SRP098795
RNA-seq data over Arabidopsis thaliana germination
  • organism-icon Arabidopsis thaliana
  • sample-icon 29 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1000

Description

RNAseq profiling of 10 time points during germination in Arabidopsis, from freshly harvested seed, through mature seed, stratification, germination and to post-germination. Overall design: Total RNA was extracted from Arabidopsis seeds at 10 time points during germination in triplicate. The time points were: freshly harvested seed (H), seeds following 15 days of ripening (0 h), seeds after; 1 h of stratification (1 h S), 12 h of stratification (12 h S), 48 h of stratification (48 h S), followed by seed collected 1 hour into the light (1 h SL), 6 hours into the light (6 h SL), 12 hours into the light (12 h SL), 24 hours into the light (24 h SL) and 48 hours into the light (48 h SL).

Publication Title

Extensive transcriptomic and epigenomic remodelling occurs during Arabidopsis thaliana germination.

Sample Metadata Fields

Specimen part, Subject, Time

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accession-icon GSE18544
Expression Profiling of a Mouse Xenograft Model of Triple-Negative Breast Cancer Brain Metastases With Vorinostat
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Gene Expression Profiling of a Mouse Xenograft Model of Triple-Negative Breast Cancer Brain Metastases With and Without Vorinostat Treatment.

Publication Title

Vorinostat inhibits brain metastatic colonization in a model of triple-negative breast cancer and induces DNA double-strand breaks.

Sample Metadata Fields

Treatment

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accession-icon GSE83586
Molecular classification of bladder cancer: global mRNA classification versus tumor cell phenotype classification.
  • organism-icon Homo sapiens
  • sample-icon 303 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

In this study gene expression profiles for 307 cases of advanced bladder cancers were compared to molecular phenotype at the tumor cell level. TUR-B tissue for RNA extraction was macrodissected from the close vicinity of the tissue sampled for immunohistochemistry to ensure high-quality sampling and to minimize the effects of intra-tumor heterogeneity. Despite excellent agreement between gene expression values and IHC-score at the single marker level, broad differences emerge when samples are clustered at the global mRNA versus tumor cell (IHC) levels. Classification at the different levels give different results in a systematic fashion, which implicates that analysis at both levels is required for optimal subtype-classification of bladder cancer.

Publication Title

Molecular classification of urothelial carcinoma: global mRNA classification versus tumour-cell phenotype classification.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE12006
Oxygen downshift experiment with E.coli W3110
  • organism-icon Escherichia coli
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Dynamical response to oxygen downshift under fermentation conditions was tested by taking sample before (S1) and after (S2, S3 and S4) the oxygen downshift. The dynamical changes relevant for ongoing research on physiology were applied.

Publication Title

Norvaline is accumulated after a down-shift of oxygen in Escherichia coli W3110.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE104922
Molecular subtype classification of urothelial carcinoma in Lynch syndrome
  • organism-icon Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We aimed to provide a molecular description of Lynch syndrome-associated urothelial cancer in relation to molecular subtypes of sporadic bladder cancer. Whole genome mRNA expression profiles of 41 tumors and immunohistochemical stainings against FGFR3, KRT5, CCNB1, RB1, and CDKN2A (p16) of 37 tumors from Lynch syndrome patients were generated. Pathological data, microsatellite instability, anatomic location, and overall survival data was analyzed and compared with data from sporadic bladder cancer.

Publication Title

Molecular subtype classification of urothelial carcinoma in Lynch syndrome.

Sample Metadata Fields

No sample metadata fields

View Samples
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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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