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accession-icon GSE2280
Prediction of lymphatic metastasis from primary squamous cell carcinoma of the oral cavity
  • organism-icon Homo sapiens
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Metastasis via the lymphatics is a major risk factor in squamous cell carcinoma of the oral cavity (OSCC). We sought to determine whether the presence of metastasis in the regional lymph node could be predicted by a gene expression signature of the primary tumor. A total of 18 OSCCs were characterized for gene expression by hybridizing RNA to Affymetrix U133A gene chips. Genes with differential expression were identified using a permutation technique and verified by quantitative RT-PCR and immunohistochemistry. A predictive rule was built using a support vector machine, and the accuracy of the rule was evaluated using crossvalidation on the original data set and prediction of an independent set of four patients. Metastatic primary tumors could be differentiated from nonmetastatic primary tumors by a signature gene set of 116 genes. This signature gene set correctly predicted the four independent patients as well as associating five lymph node metastases from the original patient set with the metastatic primary tumor group. We concluded that lymph node metastasis could be predicted by gene expression profiles of primary oral cavity squamous cell carcinomas. The presence of a gene expression signature for lymph node metastasis indicates that clinical testing to assess risk for lymph node metastasis should be possible.

Publication Title

Gene expression signature predicts lymphatic metastasis in squamous cell carcinoma of the oral cavity.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP041888
Altered epigenetic programming links intestinal inflammation to colon cancer (RNA-seq)
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

This study uses whole-transcriptome sequencing to characterize the transcriptomes of the AOM/DSS mouse model. In this model, mice are treated with dextran sodium sulfate (DSS) to induce colitis. When this treatment is preceded by injections of the weak carcinogen azoxymethane (AOM) the mice develop intestinal tumors. Our results identify sets of differentially expressed genes which are correlated with methylation changes of the corresponding genes. Overall design: Whole transcriptome analysis of Mus musculus. Three conditions were sequenced and analyzed, the first is an untreated control, the second corresponds to inflammation induced by applying DSS, the third to cancer induced by inflammation and application of AOM. The control condition as well as the AOM-induced cancer condition were analyzed using three replicates, the second condition using 4 replicates.

Publication Title

Chronic inflammation induces a novel epigenetic program that is conserved in intestinal adenomas and in colorectal cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE71997
Insights into ulcerative colitis and ileal pouchitis from a model of stasis-induced enteric dysbiosis and genetic susceptibility
  • organism-icon Mus musculus
  • sample-icon 25 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Gut dysbiosis and host genetics are implicated as causative factors in inflammatory bowel disease, yet mechanistic insights are lacking. Longitudinal analysis of ulcerative colitis patients following total colectomy with ileal anal anastomosis (IPAA) where >50% develop pouchitis, offers a unique setting to examine cause vs. effect. To recapitulate human IPAA, we employed a mouse model of surgically-created blind self-filling (SFL) and self-emptying (SEL) ileal loops. SFL exhibit fecal stasis due to directional peristalsis motility oriented towards away from the loop end, whereas SEL remain empty. In wild type mice, SFL, but not SEL, develop pouch-like microbial communities without accompanying active inflammation. However, in genetically susceptible IL-10-/- deficient mice, SFL, but not SEL, exhibit severe inflammation and mucosal transcriptomes resembling human pouchitis. Germ-free IL10-/- mice conventionalized with wild type SFL, but not SEL, microbiota, develop severe colitis. These data demonstrate an essential role for fecal stasis, gut dysbiosis, and genetic susceptibility and offer insights into human pouchitis and ulcerative colitis.

Publication Title

Insights into the pathogenesis of ulcerative colitis from a murine model of stasis-induced dysbiosis, colonic metaplasia, and genetic susceptibility.

Sample Metadata Fields

Specimen part

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accession-icon SRP158325
Reproducibility of molecular phenotypes after long-term differentiation to Human iPSC-Derived Neurons: a multi-site omics study [bulk]
  • organism-icon Homo sapiens
  • sample-icon 449 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Reproducibility in molecular and cellular studies is fundamental to scientific discovery. To establish the reproducibility of a well-defined long term neuronal differentiation protocol, we repeated the cellular and molecular comparison of the same two iPSC lines across five distinct laboratories. Despite uncovering acceptable variability within individual laboratories, we detect poor cross-site reproducibility of the differential gene expression signature between these two lines. Factor analysis identifies the laboratory as the largest source of variation along with several variation-inflating confounds such as passaging effects and progenitor storage. Single cell transcriptomics shows substantial cellular heterogeneity underlying inter-laboratory variability and being responsible for biases in differential gene expression inference. Factor analysis-based normalization of the combined dataset can remove the nuisance technical effects, enabling the execution of robust hypothesis generating studies. Our study shows that multi-center collaborations can expose systematic biases and identify critical factors to be standardized when publishing novel protocols, contributing to increased cross-site reproducibility. Overall design: RNAseq profiles of 57 bulk Human iPSC-Derived Neurons differentiated across five laboratories were generated in triplicates at two different time points and sequenced on 1 lane of HiSeq4000 at 75bp paired end. RNAseq profiles of .... single cells extracted from 2 of the 5 laboratories at the later time point were isolated by FACS onto 96-well plates and sequenced on 1 lane of HiSeq4000 at 75bp paired end.

Publication Title

Reproducibility of Molecular Phenotypes after Long-Term Differentiation to Human iPSC-Derived Neurons: A Multi-Site Omics Study.

Sample Metadata Fields

Specimen part, Cell line, Subject, Time

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accession-icon GSE53590
Dietary fat disturbance of of gut microbial diurnal patterns uncouples host metabolic networks.
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Diet-induced obesity (DIO) is rapidly becoming a global health problem, particularly as Westernization of emerging nations continues. Currently, one third of adult Americans are considered obese and, if current trends continue, >90% of US citizens are predicted to be affected by 2050. However, efforts to fight this epidemic have not yet produced sound solutions for prevention or treatment. Our studies reveal a balanced and chronobiological relationship between food consumption, daily variation in gut microbial evenness and function, basomedial hypothalamic circadian clock (CC) gene expression, and key hepatic metabolic regulatory networks , including CC and nuclear receptors (NR), that is are essential for metabolic homeostasis. Western diets high in saturated fats dramatically alter diurnal variation in microbial composition and function, which in turn lead to uncoupling of the hepatic CC and NR networks from central CC control in ways that offset the timing and types of regulatory factors directing metabolic function. These signals include microbial metabolites such as short chain fatty acids (SCFAs) and hydrogen sulfide (H2S) that can directly regulate or disrupt metabolic networks of the hepatocyte. Our study therefore provides insights into the complex and dynamic relationships between diet, gut microbes, and the host that are critical for maintenance of health. Perturbations of this constellation of processes, in this case by diet-induced dysbiosis and its metabolomic signaling, can potentially promote metabolic imbalances and disease. This knowledge opens up many possibilities for novel therapeutic and interventional strategies to treat and prevent DIO, ranging from the manipulation of gut microbial function to pharmacological targeting of host pathways to restore metabolic balance.

Publication Title

Effects of diurnal variation of gut microbes and high-fat feeding on host circadian clock function and metabolism.

Sample Metadata Fields

Specimen part

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accession-icon SRP066955
RNA-Seq of Lgr6 positive and negative cells in mouse mammary gland
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Lgr6-positive cells have been shown to label stem/progenitors cells in several tissues including tongue and skin. However their role in mammary gland has never been investigated. Here we used Lgr6-eGFP-IRES-CreER2 mice to isolate and characterize Lgr6-positive population in mammary gland of 5-week old female mice. Overall design: Examination of transcriptional differences between Lgr6 positive and negative cells

Publication Title

Lgr6 labels a rare population of mammary gland progenitor cells that are able to originate luminal mammary tumours.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon GSE15793
Expression profiling of skeletal muscle following acute 2-adrenergic stimulation
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina Mouse Ref-6 V1

Description

Systemic administration of -adrenoceptor (-AR) agonists has been found to induce skeletal muscle hypertrophy and significant metabolic changes. In the context of energy homeostasis, the importance of -AR signaling has been highlighted by the inability of 13-AR-deficient mice to regulate energy expenditure and susceptibility to diet induced obesity. However, the molecular pathways and gene expression changes that initiate and maintain these phenotypic modulations are poorly understood. Therefore, the aim of this study was to identify differential changes in gene expression in murine skeletal muscle associated with systemic acute administration of the 2-AR agonist formoterol. Skeletal muscle gene expression (from murine tibialis anterior) was profiled at both 1 and 4 hours following systemic administration of the 2-AR agonist formoterol, using 46K Illumina(R) Sentrix BeadArrays. Illumina expression profiling revealed significant expression changes in genes associated with skeletal muscle hypertrophy, myoblast differentiation, metabolism, circadian rhythm, transcription, histones, and oxidative stress.

Publication Title

Expression profiling of skeletal muscle following acute and chronic beta2-adrenergic stimulation: implications for hypertrophy, metabolism and circadian rhythm.

Sample Metadata Fields

Treatment

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accession-icon GSE94691
Gene expression of ex vivo cultured osteoclasts during the course of differentiation
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The aim of this analysis was to investigate the changes in the gene expression pattern of ex vivo cultured wildtype murine osteoclasts during the course of osteoclastogenic differentiation.

Publication Title

The Lysosomal Protein Arylsulfatase B Is a Key Enzyme Involved in Skeletal Turnover.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP066204
Next generation sequencing to elucidate the novel function of RORC (RORgamma) in breast cancer
  • organism-icon Homo sapiens
  • sample-icon 141 Downloadable Samples
  • Technology Badge IconNextSeq500

Description

Exploring the novel role of RORC (RORgamma) in breast cancer, utilizing NEXTseq with genetic gain and loss of function and pharmacological treatment. Overall design: For loss of function, control-siRNA or RORC-siRNA was transfected for 48h in three cell lines (MCF-7, T-47D and MDA-MB-231). For gain of function, CMV-empty or CMV-RORC was transfected for 48h in MDA-MB-231 cells. Furthermore, the selective RORC antagonist, SR2211 was utilized. MCF-7 cells were treated either DMSO or SR2211 (5uM) for 24h. Total RNA was extracted with the RNeasy kit. NEXTseq was performed for transcriptome analysis.

Publication Title

The Nuclear Receptor, RORγ, Regulates Pathways Necessary for Breast Cancer Metastasis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE144829
JUN induction in osteoprogenitors
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Different osteoprogenitors (SSC, BCSP, Thy+) were sorted after 2 days of JUN induction, followed by RNA extraction and microarray analysis

Publication Title

Expansion of Bone Precursors through Jun as a Novel Treatment for Osteoporosis-Associated Fractures.

Sample Metadata Fields

Specimen part

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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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