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accession-icon GSE141989
Expression data from p53 knocked-down human neuroepithelial stem (NES) cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

In this study, we take advantage of human induced pluripotent stem (iPS) cell-derived neural stem cells to study the role of p53 during human brain development. We knocked down (KD) p53 in human neuroepithelial stem (NES) cells derived from iPS cells. Upon p53KD, NES cells rapidly show centrosome amplification and genomic instability. Gene expression analysis show downregulation of genes involved in oxidative phosphorylation (OXPHOS) upon loss of p53. In addition, p53KD neural stem cells upregulate genes involved in neuronal differentiation and display an increased pace of differentiating into neurons and exhibit a phenotype corresponding to more mature neurons compared to control neurons. Taken together, this demonstrates an important role for p53 in controlling genomic stability of neural stem cells and regulation of neuronal differentiation.

Publication Title

p53 controls genomic stability and temporal differentiation of human neural stem cells and affects neural organization in human brain organoids.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE4922
Genetic Reclassification of Histologic Grade Delineates New Clinical Subtypes of Breast Cancer
  • organism-icon Homo sapiens
  • sample-icon 578 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Histological grading of breast cancer defines morphological subtypes informative of metastatic potential, although not without considerable inter-observer disagreement and clinical heterogeneity particularly among the moderately differentiated grade II (G2) tumors. We posited that a gene expression signature capable of discerning tumors of grade I (G1) and grade III (G3) histology might provide a more objective measure of grade with prognostic benefit for patients with moderately differentiated disease. To this end, we studied the expression profiles of 347 primary invasive breast tumors analyzed on Affymetrix microarrays. Using class prediction algorithms, we identified 264 robust grade-associated markers, six of which could accurately classify G1 and G3 tumors, and separate G2 tumors into two highly discriminant classes (termed G2a and G2b genetic grades) with patient survival outcomes highly similar to those with G1 and G3 histology, respectively. Statistical analysis of conventional clinical variables further distinguished G2a and G2b subtypes from each other, but also from histologic G1 and G3 tumors. In multivariate analyses, genetic grade was consistently found to be an independent prognostic indicator of disease recurrence comparable to that of lymph node status and tumor size. When incorporated into the Nottingham Prognostic Index, genetic grade enhanced detection of patients with less harmful tumors, likely to benefit little from adjuvant therapy. Our findings show that a genetic grade signature can improve prognosis and therapeutic planning for breast cancer patients, and support the view that low and high grade disease, as defined genetically, reflect independent pathobiological entities rather than a continuum of cancer progression. Three separate breast cancer cohorts were analyzed: 1) Uppsala (n=249), 2) Stockholm (n=58), 3) Singapore (n=40). The Uppsala and Singapore data can be accessed here. The Stockholm cohort data can be accessed at GEO Series GSE1456.

Publication Title

Genetic reclassification of histologic grade delineates new clinical subtypes of breast cancer.

Sample Metadata Fields

Age, Disease stage

View Samples
accession-icon GSE1456
Gene expression of breast cancer tissue in a large population-based cohort of Swedish patients
  • organism-icon Homo sapiens
  • sample-icon 316 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Tissue material was collected from all breast cancer patients receiving surgery at Karolinska Hospital from 1994-1996. Material was frozen immediatley on dry ice or in liquid nitrogen and stored in -70C freezers. This series contains expression data for n=159 tumors from which RNA could be collected in sufficient amounts and quality for analysis.

Publication Title

Gene expression profiling spares early breast cancer patients from adjuvant therapy: derived and validated in two population-based cohorts.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE2990
Gene Expression Profiling in Breast Cancer: Understanding the Molecular Basis of Histologic Grade To Improve Prognosis
  • organism-icon Homo sapiens
  • sample-icon 185 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Background: Histologic grade in breast cancer provides clinically important prognostic information. However, 30%-60% of tumors are classified as histologic grade 2. This grade is associated with an intermediate risk of recurrence and is thus not informative for clinical decision making. We examined whether histologic grade was associated with gene expression profi les of breast cancers and whether such profi les could be used to improve histologic grading.

Publication Title

Gene expression profiling in breast cancer: understanding the molecular basis of histologic grade to improve prognosis.

Sample Metadata Fields

Age, Disease stage

View Samples
accession-icon SRP058699
Gene expression of rhabdomyosarcoma cells infected with cytolytic and non-cytolytic variants of coxsackievirus B2 Ohio
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

In this study the gene expression in cells infected with lytic and non-lytic variants of coxsackievirus B2 Ohio (CVB2O) were analyzed using next generation sequencing. This approach was selected with the purpose of elucidating the effects of lytic and non-lytic viruses on host cell transcription. Total RNA was extracted from infected cells, next generation sequencing was performed, and the reads were subsequently mapped against the human and CVB2O genomes. The amount of intracellular virions was measured, showing a relative amount of virus RNA 13 times higher in the cells infected with the lytic variant, vVP1Q164K, compared to cells infected by the non-lytic CVB2Owt. Furthermore, differential gene expression in the cells infected with the two viruses was identified and a number of genes singled out as possible keys to the answer of how the viruses interact with the host cells, resulting in lytic or non-lytic infections. Overall design: 4 samples, two samples of one strain, one sample of a different strain, and one control sample

Publication Title

The Transcriptome of Rhabdomyosarcoma Cells Infected with Cytolytic and Non-Cytolytic Variants of Coxsackievirus B2 Ohio-1.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE25332
Restoring miR-200c to aggressive endometrial cancer cell line
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Using a mimic miR-200c was restored to an aggressive, Type 2 endometrial cancer cell line, Hec50

Publication Title

MicroRNA-200c mitigates invasiveness and restores sensitivity to microtubule-targeting chemotherapeutic agents.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP012147
Alkbh1/Tzfp Repress a Non-Repeat piRNA Cluster in Pachytene Spermatocytes
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Piwi proteins and Piwi-interacting small RNAs (piRNAs) have known functions in transposon silencing in the male germline of fetal and newborn mice. Both are also necessary for spermatogenesis in adult testes, however, their function here remains a mystery. Here, we use germ cell isolations and small RNA sequencing to show that most piRNAs in meiotic spermatocytes originate from clusters in intergenic non-repeat regions of DNA. The regulation of these piRNA clusters, including the processing of the precursor transcripts into individual piRNAs, is accomplished through mostly unknown processes. We present evidence for a regulatory mechanism for one such cluster, named cluster 1082B, located on chromosome 7 in the mouse genome, containing 788 unique piRNAs. The precursor transcript and individual piRNAs within the cluster are repressed by the Alkbh1 dioxygenase and the transcription repressor Tzfp, which are believed to be interaction partners in testis. We observe more than a thousand-fold upregulation of individual piRNAs in pachytene spermatocytes isolated from Alkbh1-/- and TzfpGTi/GTi testes. Repression is further supported by the identification of a 10 bp Tzfp recognition sequence contained within the precursor transcript. Downregulation of long interspersed elements 1 (LINE1) and intracisternal A-particle (IAP) transcripts in the Alkbh1-/- and TzfpGTi/GTi testes leads us to propose a potential role for the 1082B-encoded piRNAs in transposon silencing. Overall design: Characterization of small RNAs in mouse pachytene spermatocytes for wild-type (WT) and Alkbh1-/- and TzfpGTi/GTi, and mRNA in mouse pachytene spermatocytes for wild-type (WT) and Alkbh1-/-

Publication Title

Alkbh1 and Tzfp repress a non-repeat piRNA cluster in pachytene spermatocytes.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE26188
Liver gene expression in animals with hepatocyte-specific deletion of JAK2
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Growth hormone signaling in hepatocytes is fundamentally important. Disruptions in this pathway have led to fatty liver and other metabolic abnormalities. Growth hormone signals through the JAK2/STAT5 pathway. Mice with hepatocyte specific deletion of STAT5 were previously shown to develop fatty liver. Our aim in this study was to determine the effect of deleting JAK2 in hepatocytes on liver gene expression. To do so, we generated animals with hepatocyte specific deletion of JAK2.

Publication Title

Abrogation of growth hormone secretion rescues fatty liver in mice with hepatocyte-specific deletion of JAK2.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE74625
KLF15
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2), Agilent-014868 Whole Mouse Genome Microarray 4x44K G4122F (Probe Name version)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Glucocorticoids enhance muscle endurance and ameliorate Duchenne muscular dystrophy through a defined metabolic program.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE74623
Transcriptional effects of forced KLF15 over-expression in mouse muscle.
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Excessive or sustained glucocorticoid (GC) exposure causes muscle wasting. Paradoxically, moderate or transient GC exposure elicits ergogenic effects, evidenced by their widespread use as doping agents by endurance athletes and poorly understood efficacy in Duchenne muscular dystrophy (DMD), a genetic muscle wasting disease. While mechanisms underlying GC-mediated muscle wasting are well defined, the molecular basis for the latter remains unknown. In this arm of our studies, we compare expression profiles in quadriceps tissue from KLF15 transgenic (MTg) and non-Tg mice.

Publication Title

Glucocorticoids enhance muscle endurance and ameliorate Duchenne muscular dystrophy through a defined metabolic program.

Sample Metadata Fields

Specimen part

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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