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accession-icon GSE20076
BRD7 is a candidate tumour suppressor gene required for p53 function
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

Oncogene-induced senescence (OIS) is a p53-dependent defence mechanism against uncontrolled proliferation. Consequently, many human tumours harbour p53 mutations while others show a dysfunctional p53 pathway, frequently by unknown mechanisms. We identified BRD7, a bromodomain-containing protein whose inhibition allows full neoplastic transformation in the presence of wild-type p53. Intriguingly, in human breast tumours harbouring wild-type, but not mutant p53, the BRD7 gene locus was frequently deleted and low BRD7 expression was found in a subgroup of tumours. Functionally, BRD7 is required for efficient p53-mediated transcription of a subset of target genes. BRD7 interacts with p53 and p300, and is recruited to target gene promoters, affecting histone acetylation, p53 acetylation, and promoter activity. Thus, BRD7 suppresses tumourigenicity by serving as a p53 cofactor required for efficient induction of p53-dependent OIS.

Publication Title

BRD7 is a candidate tumour suppressor gene required for p53 function.

Sample Metadata Fields

Specimen part, Disease, Cell line

View Samples
accession-icon GSE14627
Gene expression analysis of SH-SY5Y neuroblastoma cells overexpressing ZNF423
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

We have identified ZNF423 (also known as Ebfaz, OAZ or Zfp423) as a component critically required for retinoic acid (RA)-induced differentiation. ZNF423 associates with the RAR/RXR nuclear receptor complex and is essential for transactivation in response to retinoids. Down-regulation of ZNF423 expression by RNA interference in neuroblastoma cells results in a growth advantage and resistance to RA-induced differentiation, whereas overexpression of ZNF423 leads to growth inhibition and enhanced differentiation. Futhermore, we show that low ZNF423 expression is associated with poor disease outcome of neuroblastoma patients. To identify the other key pathways regulated by ZNF423 in human neuroblastoma, we expressed elevated levels of ZNF423 in SH-SY5Y cells and performed full genome gene expression analysis in these cells.

Publication Title

ZNF423 is critically required for retinoic acid-induced differentiation and is a marker of neuroblastoma outcome.

Sample Metadata Fields

Specimen part

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accession-icon GSE79372
Pretreatment microRNA Expression Impacting on Epithelial-to-Mesenchymal Transition Predicts Intrinsic Radiosensitivity in Head and Neck Cancer Cell Lines and Patients
  • organism-icon Homo sapiens
  • sample-icon 98 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip, Illumina HumanWG-6 v3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Pretreatment microRNA Expression Impacting on Epithelial-to-Mesenchymal Transition Predicts Intrinsic Radiosensitivity in Head and Neck Cancer Cell Lines and Patients.

Sample Metadata Fields

Sex, Specimen part, Cell line

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accession-icon GSE79368
Pretreatment microRNA Expression Impacting on Epithelial-to-Mesenchymal Transition Predicts Intrinsic Radiosensitivity in Head and Neck Cancer Cell Lines and Patients [mRNA expression]
  • organism-icon Homo sapiens
  • sample-icon 96 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

Purpose: Predominant causes of head and neck cancer recurrence after radiotherapy are rapid repopulation, hypoxia, fraction of cancer stem cells and intrinsic radioresistance. Currently, intrinsic radioresistance can only be assessed by ex-vivo colony assays. Besides being time-consuming, colony assays do not identify causes of intrinsic resistance. We aimed to identify a biomarker for intrinsic radioresistance to be used before start of treatment and to reveal biological processes that could be targeted to overcome intrinsic resistance.

Publication Title

Pretreatment microRNA Expression Impacting on Epithelial-to-Mesenchymal Transition Predicts Intrinsic Radiosensitivity in Head and Neck Cancer Cell Lines and Patients.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE79371
Pretreatment microRNA expression impacting on epithelial to mesenchymal transition predicts intrinsic radiosensitivity in head and neck cancer cell lines and patients [FaDu]
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

Purpose: Predominant causes of head and neck cancer recurrence after radiotherapy are rapid repopulation, hypoxia, fraction of cancer stem cells and intrinsic radioresistance. Currently, intrinsic radioresistance can only be assessed by ex-vivo colony assays. Besides being time-consuming, colony assays do not identify causes of intrinsic resistance. We aimed to identify a biomarker for intrinsic radioresistance to be used before start of treatment and to reveal biological processes that could be targeted to overcome intrinsic resistance.

Publication Title

Pretreatment microRNA Expression Impacting on Epithelial-to-Mesenchymal Transition Predicts Intrinsic Radiosensitivity in Head and Neck Cancer Cell Lines and Patients.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE103117
Genome-wide analysis of bacterial determinants of plant growth promotion and induced systemic resistance by Pseudomonas fluorescens
  • organism-icon Arabidopsis thaliana
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Pseudomonas fluorescens strain SS101 (Pf.SS101) promotes growth of Arabidopsis thaliana, enhances greening and lateral root formation, and induces systemic resistance (ISR) against the bacterial pathogen Pseudomonas syringae pv. tomato (Pst). Here, targeted and untargeted approaches were adopted to identify bacterial determinants and underlying mechanisms involved in plant growth promotion and ISR by Pf.SS101. Based on targeted analyses, no evidence was found for volatiles, lipopeptides and siderophores in plant growth promotion by Pf.SS101. Untargeted, genome-wide analyses of 7,488 random transposon mutants of Pf.SS101 led to the identification of 21 mutants defective in both plant growth promotion and ISR. Many of these mutants, however, were auxotrophic and impaired in root colonization. Genetic analysis of three mutants followed by site-directed mutagenesis, genetic complementation and plant bioassays revealed the involvement of the phosphogluconate dehydratase gene edd, the response regulator gene colR and the adenylsulfate reductase gene cysH in both plant growth promotion and ISR. Subsequent comparative plant transcriptomics analyses strongly suggest that modulation of sulfur assimilation, auxin biosynthesis and transport, steroid biosynthesis and carbohydrate metabolism in Arabidopsis are key mechanisms linked to growth promotion and ISR by Pf.SS101.

Publication Title

Genome-wide analysis of bacterial determinants of plant growth promotion and induced systemic resistance by Pseudomonas fluorescens.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE119135
Transcriptomic profiles of tissues from rats treated with drug combinations
  • organism-icon Rattus norvegicus
  • sample-icon 866 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age, Specimen part, Time

View Samples
accession-icon GSE119133
Transcriptomic profiles of tissues from rats treated with drug combinations [Study 3]
  • organism-icon Rattus norvegicus
  • sample-icon 290 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Combinations of anticancer agents may have synergistic anti-tumor effects, but enhanced toxicity often limit their clinical use. The risk that combinations of two or more drugs will cause adverse effects that are more severe than drugs used as monotherpies can be hypothesized from comprehensive analysis of each compounds activity. We generated microarray gene expression data following a single dose of agents administered individually with that of the agents administered in a combination. The key objective of this initiative is to generate and make publicly available key high-content gene expression data sets for mechanistic hypothesis generation for several anticancer drug combinations. The expectation is that availability of tissue-based genomic information that are derived from target tissues will facilitate the generation and testing of mechanistic hypotheses. The view is that availability of these data sets for bioinformaticians and other scientists will contribute to analysis of these data and evaluation of the approach.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Time

View Samples
accession-icon GSE119122
Transcriptomic profiles of tissues from rats treated with drug combinations [Study 1]
  • organism-icon Rattus norvegicus
  • sample-icon 288 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Combinations of anticancer agents may have synergistic anti-tumor effects, but enhanced toxicity often limit their clinical use. The risk that combinations of two or more drugs will cause adverse effects that are more severe than drugs used as monotherpies can be hypothesized from comprehensive analysis of each compounds activity. We generated microarray gene expression data following a single dose of agents administered individually with that of the agents administered in a combination. The key objective of this initiative is to generate and make publicly available key high-content gene expression data sets for mechanistic hypothesis generation for several anticancer drug combinations. The expectation is that availability of tissue-based genomic information that are derived from target tissues will facilitate the generation and testing of mechanistic hypotheses. The view is that availability of these data sets for bioinformaticians and other scientists will contribute to analysis of these data and evaluation of the approach.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Time

View Samples
accession-icon GSE119129
Transcriptomic profiles of tissues from rats treated with drug combinations [Study 2]
  • organism-icon Rattus norvegicus
  • sample-icon 288 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Combinations of anticancer agents may have synergistic anti-tumor effects, but enhanced toxicity often limit their clinical use. The risk that combinations of two or more drugs will cause adverse effects that are more severe than drugs used as monotherpies can be hypothesized from comprehensive analysis of each compounds activity. We generated microarray gene expression data following a single dose of agents administered individually with that of the agents administered in a combination. The key objective of this initiative is to generate and make publicly available key high-content gene expression data sets for mechanistic hypothesis generation for several anticancer drug combinations. The expectation is that availability of tissue-based genomic information that are derived from target tissues will facilitate the generation and testing of mechanistic hypotheses. The view is that availability of these data sets for bioinformaticians and other scientists will contribute to analysis of these data and evaluation of the approach.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age, Specimen part, Time

View Samples
...

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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Developed by the Childhood Cancer Data Lab

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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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