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accession-icon SRP071214
Sox2 is the determining oncogenic switch in promoting lung squamous cell carcinoma from different cells-of-origin
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Squamous cell carcinoma (SCC) of lung is a devastating malignancy with no effective treatments, due to its complex genomic profile. Therefore, pre-clinical models mimicking its salient features are urgently needed. Here we describe mouse models bearing various combinations of genetic lesions predominantly found in human SCC. We show that Sox2 but not Fgfr1 overexpression in tracheobronchial basal cells combined with Cdkn2ab and Pten loss results in SCC closely resembling the human counterpart. Interestingly, Sox2;Pten;Cdkn2ab mice develop SCC with a more peripheral location when Club or Alveolar type 2 (AT2) cells are targeted. Our model highlights the essential role of Sox2 in promoting a squamous cell fate from different cells-of-origin and represents an invaluable tool for the developing better intervention strategies. Overall design: After RNA extraction and Bioanalyzer analysis, we processed samples with high quality RNA profiles using Illumina Hiseq2500.

Publication Title

SOX2 Is the Determining Oncogenic Switch in Promoting Lung Squamous Cell Carcinoma from Different Cells of Origin.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Subject

View Samples
accession-icon SRP075828
NFIB is a driver of SCLC initiation, progression and metastasis in mouse and marks metastatic disease in patients
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Small Cell Lung Cancer (SCLC) is the most aggressive type of lung cancer with early metastatic dissemination and invariable development of resistant disease for which no effective treatment is available to date. Mouse models of SCLC based on inactivation of Rb1 and Trp53 developed earlier showed frequent amplifications of two transcription factor genes: Nfib and Mycl. Overexpression of Nfib but not Mycl in SCLC mouse results in an enhanced and altered metastatic profile, and appears to be associated with genomic instability. NFIB promotes tumor heterogeneity with the concomitant expansive growth of poorly differentiated, highly proliferative, and invasive tumor cell populations. Consistent with the mouse data, NFIB expression in high-grade human neuroendocrine carcinomas correlates with advanced stage III/IV disease warranting its further assessment as a potentially valuable progression marker in a clinical setting. Overall design: Genomic DNA from mouse small cell lung tumor samples was analyzed by mate pair sequencing and low coverage sequencing. And RNA from Nfib overexpressing mouse small cell lung cancer cell lines was further analyzed for high quality RNA profiles using Illumina Hiseq2500. This series contains only RNA-seq data.

Publication Title

Transcription Factor NFIB Is a Driver of Small Cell Lung Cancer Progression in Mice and Marks Metastatic Disease in Patients.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE51130
Using a rhabdomyosarcoma patient-derived xenograft to examine precision medicine approaches and model acquired resistance
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Original patient tumor is directly implanted in mice xenografts. Tumor is propagated to multiple mice for conduct of 6 arm treatment trials and control. Therapies are selected based on T0 and F0 genomic profiles.

Publication Title

Using a rhabdomyosarcoma patient-derived xenograft to examine precision medicine approaches and model acquired resistance.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE50208
Molecular-guided therapy predictions reveal drug resistance phenotypes and treatment alternatives in malignant peripheral nerve sheath tumors
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Use existing public data, cell lines and patient tumors with a personalized medicine approach to predict effective therapies for treatment of Neurofibroma tumors.

Publication Title

Molecular-guided therapy predictions reveal drug resistance phenotypes and treatment alternatives in malignant peripheral nerve sheath tumors.

Sample Metadata Fields

Specimen part

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accession-icon GSE48009
Gene expression in IRfl/fl Cre- and IRfl/fl Cre+ mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The floxed insulin receptor was specifically targetted for deletion in the mammary gland using a mouse strain bearing Cre recombinase under the BLG promoter.

Publication Title

The insulin receptor plays an important role in secretory differentiation in the mammary gland.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP169609
Selective roles of vertebrate PCF11 in premature and full-length transcript termination (chromatin-bound RNA-seq)
  • organism-icon Homo sapiens
  • sample-icon 96 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

The pervasive nature of RNA polymerase II (Pol II) transcription requires efficient termination. A key player in this process is the cleavage and polyadenylation (CPA) factor PCF11, which directly binds to the Pol II C-terminal domain and dismantles elongating Pol II from DNA in vitro. We demonstrate that PCF11-mediated termination is essential for vertebrate development. A range of genomic analyses, including: mNET-seq, 3' mRNA-seq, chromatin RNA-seq and ChIP-seq, reveals that PCF11 enhances transcription termination and stimulates early polyadenylation genome-wide. PCF11 binds preferentially between closely spaced genes, where it prevents transcriptional interference and downstream gene silencing. Notably, PCF11 is sub-stoichiometric to the CPA complex. Low levels of PCF11 are maintained by an auto-regulatory mechanism involving premature termination of its own transcript, and are important for normal development. Both in human cell culture and during zebrafish development, PCF11 selectively attenuates the expression of other transcriptional regulators by premature CPA and termination. Overall design: Semi-nascent transcriptome measured by chromatin-bound RNA-seq in HeLa cells. Control and PCF11 knock-down (2 biological replicates) and control and PCF11 PAS1 deletion (4 biological replicates).

Publication Title

Selective Roles of Vertebrate PCF11 in Premature and Full-Length Transcript Termination.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon SRP175015
Selective roles of vertebrate PCF11 in premature and full-length transcript termination (zebrafish 3' mRNA-seq)
  • organism-icon Danio rerio
  • sample-icon 56 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The pervasive nature of RNA polymerase II (Pol II) transcription requires efficient termination. A key player in this process is the cleavage and polyadenylation (CPA) factor PCF11, which directly binds to the Pol II C-terminal domain and dismantles elongating Pol II from DNA in vitro. We demonstrate that PCF11-mediated termination is essential for vertebrate development. A range of genomic analyses, including: mNET-seq, 3' mRNA-seq, chromatin RNA-seq and ChIP-seq, reveals that PCF11 enhances transcription termination and stimulates early polyadenylation genome-wide. PCF11 binds preferentially between closely spaced genes, where it prevents transcriptional interference and downstream gene silencing. Notably, PCF11 is sub-stoichiometric to the CPA complex. Low levels of PCF11 are maintained by an auto-regulatory mechanism involving premature termination of its own transcript, and are important for normal development. Both in human cell culture and during zebrafish development, PCF11 selectively attenuates the expression of other transcriptional regulators by premature CPA and termination. Overall design: 3' mRNA-seq in individual zebrafish embryo heads. Two types of mutants: zPCF11 null and zPCF11 with deletion of PAS1. Wild-type (wt, +/+), heterozygous (het, +/-) and homozygous mutant (hom, -/-) embryos were analyzed. Wild-type and heterozygous animals were phenotypically indistinguishable.

Publication Title

Selective Roles of Vertebrate PCF11 in Premature and Full-Length Transcript Termination.

Sample Metadata Fields

Subject

View Samples
accession-icon SRP175016
Selective roles of vertebrate PCF11 in premature and full-length transcript termination (human 3' mRNA-seq)
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The pervasive nature of RNA polymerase II (Pol II) transcription requires efficient termination. A key player in this process is the cleavage and polyadenylation (CPA) factor PCF11, which directly binds to the Pol II C-terminal domain and dismantles elongating Pol II from DNA in vitro. We demonstrate that PCF11-mediated termination is essential for vertebrate development. A range of genomic analyses, including: mNET-seq, 3' mRNA-seq, chromatin RNA-seq and ChIP-seq, reveals that PCF11 enhances transcription termination and stimulates early polyadenylation genome-wide. PCF11 binds preferentially between closely spaced genes, where it prevents transcriptional interference and downstream gene silencing. Notably, PCF11 is sub-stoichiometric to the CPA complex. Low levels of PCF11 are maintained by an auto-regulatory mechanism involving premature termination of its own transcript, and are important for normal development. Both in human cell culture and during zebrafish development, PCF11 selectively attenuates the expression of other transcriptional regulators by premature CPA and termination. Overall design: 3' mRNA-seq in HeLa cells. Control and PCF11 knock-down (4 biological replicates); control and PCF11 PAS1 deletion clones muA and muB (3 biological replicates); control and additional PCF11 PAS1 deletion clones muC and muD (1 replicate).

Publication Title

Selective Roles of Vertebrate PCF11 in Premature and Full-Length Transcript Termination.

Sample Metadata Fields

Subject

View Samples
accession-icon GSE69524
NCI Sarcoma Cell Line Panel
  • organism-icon Homo sapiens
  • sample-icon 75 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [HuEx-1_0-st-v2,coreR3,A20071112,EP.cdf (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Sarcoma Cell Line Screen of Oncology Drugs and Investigational Agents Identifies Patterns Associated with Gene and microRNA Expression.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE68591
Exon expression for NCI Sarcoma cell line panel
  • organism-icon Homo sapiens
  • sample-icon 75 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [HuEx-1_0-st-v2,coreR3,A20071112,EP.cdf (huex10st)

Description

Characterization of 68 cell lines derived from human sarcoma and 5 normal counterpart cells, including drug sensitivity testing, gene expression profiling and microRNA expression profiling have been completed. Data and tools for searching these data will be made publicly available through the NCI Developmental Therapeutics Program. The raw data (.cel files ) are provided through the GEO website. Sarcoma represents a variety of cancers at arise from cells of mesenchymal origin and have seen limited treatment advances in the last decade. Drug sensitivity data coupled with the transcription and microRNA profiles of a cohort of sarcoma cell lines may help define novel treatment paradigms.

Publication Title

Sarcoma Cell Line Screen of Oncology Drugs and Investigational Agents Identifies Patterns Associated with Gene and microRNA Expression.

Sample Metadata Fields

No sample metadata fields

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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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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