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accession-icon GSE40280
Gene expression profile after TRPV4 knockdown in 3T3-F442A adipocytes
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Comparing gene expression profile in 3T3-F442A adipocytes with shRNA against TRPV4 or GFP. TRPV4 is an ion channel expressed in adipocytes. Results provided information that how loss-of-function of TRPV4 affects gene expression in adipocytes.

Publication Title

TRPV4 is a regulator of adipose oxidative metabolism, inflammation, and energy homeostasis.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP072851
Transcriptionally inactive ATF2 variant drives melanomagenesis [Seq]
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

Characterized by striking metastatic propensity and chemoresistance, melanoma is among the most lethal cutaneous malignancies. The transcription factor ATF2 was shown to elicit oncogenic activities in melanoma, and its inhibition attenuates melanoma development. Here, a mouse model engineered to express a transcriptionally inactive form of Atf2 (Atf2?8,9) was found to be sufficient to induce nevi formation and, when crossed with BrafV600E animals, to promote melanoma development. The cross of Atf2?8,9 with BrafV600E;Pten-/- mice augmented pigmentation, tumorigenicity, and metastasis. Similar to mouse Atf2?8,9, the human ATF2 splice variant 5 enhanced growth and migration capacity of cultured melanoma and immortalized melanocytes. Induced Melan-A, CXCL9, S100A8, CCR7 expression, seen in Atf2?8,9-driven tumors associate with their enhanced pigmentation, immune infiltration and propensity to metastasize. Notably, elevated ATF2SV5 expression in melanoma specimens coincided with poor prognosis. The gain-of-function activity elicited by the truncated ATF2 form offers unexpected insight into mechanisms underlying melanoma development and progression. Overall design: Compared silencing of ATF2SV5 in H3A cells vs. silencing of ATF2WT via Ampliseq whole transcriptome analysis on the Ion Proton

Publication Title

A Transcriptionally Inactive ATF2 Variant Drives Melanomagenesis.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP154372
Differential gene expression in NPHS2-Cre +/+ mouse glomeruli versus wild-type control
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

To investigate differential gene expression that might account for the differing glomerular phenotype of NPHS2-Cre +/+ mice when compared with wild-type control, including altered GBM thickness, loss of normal foot process morphology, and decrease in podocyte number, RNA sequencing analysis was performed on glomeruli extracted from both NPHS2-Cre +/+ and wild-type control mice. Overall design: Following isolation of glomeruli using Dynabeads from NPHS2-Cre +/+ and wild-type control mice (n=2 biological replicates per genotype, singly isolated), total RNA was extracted and RNA samples were submited for sample preparation and sequencing.

Publication Title

Podocyte-specific expression of Cre recombinase promotes glomerular basement membrane thickening.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, Subject

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accession-icon GSE17735
Analysis of altered gene expressions in valproate-treated Disc1-L100P mutant mice
  • organism-icon Mus musculus
  • sample-icon 69 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Microarray analysis revealed that changes in genes expressions are brain region-dependent; expression of several genes are affected by point mutation L100P, which was verified by RT-PCR (Lcn2, Cyr61, Slc6a12, Slc40a1, Egr2), a few genes are affected by genotype and valproate (Dusp1 and Purb), suggesting their role in valproate-induced benificial effect on sensorimotor gaiting in Disc1-L100P mutant mice. The final conclusion will be drawn after series of RT-PCR confirmation.

Publication Title

Genetic and pharmacological evidence for schizophrenia-related Disc1 interaction with GSK-3.

Sample Metadata Fields

Sex, Specimen part, Compound

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accession-icon SRP056114
Amydala transcriptome changes in germ-free mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We sequenced mRNA from 12 samples extracted from mouse amygdala tissue to generate the first amygdala-specific murine transcriptome for germ-free mice (GF), conventionally raised controls (CON) and germ-free mice that have been colonized with normal microbiota from postnatal day 21 (exGF). Overall design: Equal amounts of RNA from two to three animals were pooled to yield 4 samples per group (CON, GF, and exGF). Pairwise comparisons for CONvsGF, CONvsexGF, GFvsexGF were performed using DESeq2.

Publication Title

Microbes & neurodevelopment--Absence of microbiota during early life increases activity-related transcriptional pathways in the amygdala.

Sample Metadata Fields

No sample metadata fields

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accession-icon E-MEXP-313
Transcription profiling of human T-ALL patients at diagnosis and relapse
  • organism-icon Homo sapiens
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

A "Cartes d'Identite des Tumeurs" (CIT) project from the french Ligue Nationale Contre le Cancer (<a href="http://cit.ligue-cancer.net" target="_blank">http://cit.ligue-cancer.net</a>). 104 samples; Affymetrix U133A micro-arrays.<br></br> <br></br> Ninety two patients with T-ALL were diagnosed and treated at Saint-Louis hospital, Paris. Seven patients were studied at diagnosis and relapse (total 99 T-ALL samples). There were 56 children (median age 9 years old; range 1 to 16), and 36 adults (median age 27; range 17 to 66). Informed consent was obtained from the patients and/or relatives. T-ALL diagnosis was based on morphological and immunophenotypical criteria using flow cytometry and an extended monoclonal antibody panel.<br></br> <br></br> Using a combination of molecular cytogenetic and large-scale expression analysis in human T-ALL, we identified and characterized a new recurrent chromosomal translocation, targeting the major homeobox gene cluster HOXA and the TCRB locus. Specific quantitative PCR analysis showed that the expression of the whole HOXA gene cluster was dramatically dysregulated in the HOXA-rearranged cases, and also in MLL and CALM-AF10-related T-ALL cases, strongly suggesting that HOXA genes are oncogenic in these leukemias. Inclusion of HOXA-translocated cases in a general molecular portrait of 92 T-ALL based on large-scale expression analysis shows that this rearrangement defines a new homogeneous subgroup, which shares common biological networks with the TLX1 and TLX3-related cases. Since T-ALLs derive from T-cell progenitors, expression profiles of the distinct T-ALL subgroups were analyzed with respect to those of normal human thymic sub-populations. Inappropriate utilization or perturbation of specific molecular networks involved in thymic differentiation was detected. Moreover, we found a significant association between T-ALL oncogenic subgroups and ectopic expression of a limited set of genes, including several developmental genes, namely HOXA, TLX1, TLX3, NKX3-1, SIX6 and TFAP2C. These data strongly support the view that the abnormal expression of developmental genes, including the prototypical homeobox genes HOXA, is critical in T-ALL oncogenesis.<br></br> <br></br> Project Leader: <br></br> FranC'ois Sigaux<br></br> Institut Universitaire d'Hematologie<br></br> Hopital Saint Louis, Paris, France<br></br> <br></br> Data submission:<br></br>Fabien Petel

Publication Title

HOXA genes are included in genetic and biologic networks defining human acute T-cell leukemia (T-ALL).

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage, Subject

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accession-icon GSE18644
Expression analysis in yeast model of Huntington's disease (HD)
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

Expressing a mutant fragment of huntingtin (Htt) in yeast produces several HD-relevant phenotypes. We used microarrays to study global change in expression induced by this mutant htt fragment.

Publication Title

Functional gene expression profiling in yeast implicates translational dysfunction in mutant huntingtin toxicity.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE6632
Hepatocellular carcinoma follows loss of liver-gender specificity in mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We are investigating hepatic transcriptional responses associated with castration and tumorigenic hepatitis induced by Helicobacter hepaticus infection in mature male A/JCr mice

Publication Title

Hepatocellular carcinoma associated with liver-gender disruption in male mice.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE28691
Characterization of an Oxaliplatin Sensitivity Predictor in a preclinical Murine Model of Colorectal Cancer
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Despite advances in contemporary chemotherapeutic strategies, long term survival still remains elusive for patients with metastatic colorectal cancer. A better understanding of the molecular markers of drug sensitivity to match therapy with patient is needed to improve clinical outcomes. In this study, we used in vitro drug sensitivity data from the NCI-60 cell lines together with their Affymetrix microarray data to develop a gene expression signature to predict sensitivity to oxaliplatin. In order to validate our oxaliplatin sensitivity signature, Patient-Derived Colorectal Cancer Explants (PDCCEs) were developed in NOD-SCID mice from resected human colorectal tumors. Analysis of gene expression profiles found similarities between the PDCCEs and their parental human tumors, suggesting their utility to study drug sensitivity in vivo. The oxaliplatin sensitivity signature was then validated in vivo with response data from 14 PDCCEs treated with oxaliplatin and was found to have an accuracy of 92.9% (Sensitivity=87.5%; Specificity=100%). Our findings suggest that PDCCEs can be a novel source to study drug sensitivity in colorectal cancer. Furthermore, genomic-based analysis has the potential to be incorporated into future strategies to optimize individual therapy for patients with metastatic colorectal cancer.

Publication Title

Characterization of an oxaliplatin sensitivity predictor in a preclinical murine model of colorectal cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE136287
Transcriptomic characterisation of ALDH+ cells in therapy resistant breast cancer patient samples
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This study is part of a larger multidisciplinary study entitled A dormant sub-population expressing interleukin-1 receptor characterises anti-estrogen resistant ALDH+ breast cancer stem cells.

Publication Title

Increased Expression of Interleukin-1 Receptor Characterizes Anti-estrogen-Resistant ALDH<sup>+</sup> Breast Cancer Stem Cells.

Sample Metadata Fields

Specimen part, 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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