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accession-icon GSE41258
Expression data from colorectal cancer patients
  • organism-icon Homo sapiens
  • sample-icon 389 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

The study consist of patients who presented at Memorial Sloan-Kettering Cancer Center with a colonic neoplasm between 1992 and 2004. Biological specimens used in this study include primary colon adenocarcinomas, adenomas, metastasis and corresponding normal mucosae.

Publication Title

Association of survival and disease progression with chromosomal instability: a genomic exploration of colorectal cancer.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, Subject

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accession-icon GSE17459
Down's syndrome with acute lymphoblastic pediatric leukemia (DS-ALL)
  • organism-icon Homo sapiens
  • sample-icon 119 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

DS-ALL is a highly heterogeneous disease with predominance of an aberrant exp. of CRLF2 cooperating with mutated JAK2

Publication Title

Down syndrome acute lymphoblastic leukemia, a highly heterogeneous disease in which aberrant expression of CRLF2 is associated with mutated JAK2: a report from the International BFM Study Group.

Sample Metadata Fields

Specimen part

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accession-icon GSE52824
Derivation of novel human ground state nave pluripotent stem cells.
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 12 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

Derivation of novel human ground state naive pluripotent stem cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE49767
Deterministic direct reprogramming of somatic cells to pluripotency
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Corrigendum: Deterministic direct reprogramming of somatic cells to pluripotency.

Sample Metadata Fields

Specimen part

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accession-icon GSE50131
The transcription program of Runx3 in natural killer cells and CD8+ T cells
  • organism-icon Mus musculus
  • sample-icon 28 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

Runx3-mediated transcriptional program in cytotoxic lymphocytes.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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accession-icon GSE41050
Epigenetic polymorphism and the stochastic formation of differentially methylated regions in normal and cancerous tissues
  • organism-icon Homo sapiens
  • sample-icon 14 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

Epigenetic polymorphism and the stochastic formation of differentially methylated regions in normal and cancerous tissues.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE37822
The H3K27 demethylase Utx facilitates somatic and germ cell epigenetic reprogramming to pluripotency
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The H3K27 demethylase Utx regulates somatic and germ cell epigenetic reprogramming.

Sample Metadata Fields

Specimen part

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accession-icon GSE23038
Normal prostate cells were immortalized and cultured for 650 days till several transformation hallmarks were observed
  • organism-icon Homo sapiens
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Duplication of chromosomal arm 20q occurs in prostate, cervical, colon, gastric, bladder, melanoma, pancreas and breast cancer, suggesting that 20q amplification may play a key causal role in tumorigenesis. According to an alternative view, chromosomal instabilities are mainly a common side effect of cancer progression. To test whether a specific genomic aberration might serve as a cancer initiating event, we established an in vitro system that models the evolutionary process of early stages of prostate tumor formation; normal prostate cells were immortalized and cultured for 650 days till several transformation hallmarks were observed. Gene expression patterns were measured and chromosomal aberrations were monitored by spectral karyotype analysis at different times. Several chromosomal aberrations, in particular duplication of chromosomal arm 20q, occurred early in the process and were fixed in the cell populations, while other aberrations became extinct shortly after their appearance. A wide range of bioinformatic tools, applied to our data and to data from several cancer databases, revealed that spontaneous 20q amplification can promote cancer initiation. Our computational model suggests that deregulation of some key pathways, such as MAPK, p53, cell cycle regulation and Polycomb group factors, in addition to activation of several genes like Myc, AML, B-Catenin and the ETS family transcription factors, are key steps in cancer development driven by 20q amplification. Finally we identified 13 cancer initiating genes, located on 20q13, which were significantly overexpressed in many tumors, with expression levels correlated with tumor grade and outcome; these probably play key roles in inducing malignancy via20q amplification.

Publication Title

Amplification of the 20q chromosomal arm occurs early in tumorigenic transformation and may initiate cancer.

Sample Metadata Fields

Specimen part

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accession-icon GSE53405
Circadian regulation of EGF-receptor signaling by glucocorticoids
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

Transcriptional responses to stimuli are regulated by tuning rates of transcript production and degradation. Here we show that stimulation-induced changes in transcript production and degradation rates can be inferred from simultaneously measured precursor mRNA (pre-mRNA) and mature mRNA profiles. Our studies on the transcriptome-wide responses to extracellular stimuli in different cellular model systems revealed hitherto unanticipated dynamics of transcript production and degradation rates. Intriguingly, genes with similar mRNA profiles often exhibit marked differences in the amplitude and onset of their production. Moreover, we identify a group of genes, which take advantage of the unexpectedly large dynamic range of production rates to expedite their induction by a transient production overshoot. These findings provide an unprecedented quantitative view on processes governing transcriptional responses, and may have broad implications for understanding their regulation at the transcriptional and post-transcriptional levels.

Publication Title

No associated publication

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE78757
Cortical transcriptional changes in a chemically-induced neuronopathic Gaucher disease mouse model
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Great interest has been shown in understanding the pathology of Gaucher disease (GD) due to the recently-discovered genetic relationship with Parkinsons disease. For such studies, suitable animal models of GD are required. Chemical induction of GD by inhibition of acid -glucosidase (GCase) using the irreversible inhibitor, conduritol-B-epoxide (CBE), is particularly attractive, although few systematic studies examining the effect of CBE on development of symptoms associated with neurological forms of GD have been performed. We now demonstrate a correlation between the amount of CBE injected into mice and levels of accumulation of the GD substrates, glucosylceramide and glucosylsphingosine, and show that disease pathology, indicated by altered levels of pathological markers, depends on the dose of CBE and its time of injection. Gene array analysis shows a remarkable similarly in the gene expression profile of CBE-treated mice and a genetic GD mouse model, the Gbaflox/flox;nestin-Cre mouse, with 120 of the 144 genes up-regulated in CBE-treated mice also up regulated in Gbaflox/flox;nestin-Cre mice. Finally, we demonstrate that some aspects neuropathology and some behavioral abnormalities can be arrested upon cessation of CBE treatment during a specific time window. Together, our data demonstrate that injection of mice with CBE provides a rapid and relatively easy way to induce symptoms typical of neuronal forms of GD, which will prove particularly useful when examining the role of specific biochemical pathways in GD pathology, since CBE can be injected into mice defective in components of putative pathological pathways, alleviating the need for time consuming crossing of mice.

Publication Title

Identification of Modifier Genes in a Mouse Model of Gaucher Disease.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage

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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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