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accession-icon GSE66072
Mcl-1 is a key determinant of breast cancer cell survival
  • organism-icon Homo sapiens
  • sample-icon 93 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

MCL-1 Is a Key Determinant of Breast Cancer Cell Survival: Validation of MCL-1 Dependency Utilizing a Highly Selective Small Molecule Inhibitor.

Sample Metadata Fields

Cell line

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accession-icon GSE66071
Mcl-1 is a key determinant of breast cancer cell survival [expression]
  • organism-icon Homo sapiens
  • sample-icon 93 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

mRNA expression profile of cultured Breast Cancer cell line measured by Affymetrix microarrays

Publication Title

MCL-1 Is a Key Determinant of Breast Cancer Cell Survival: Validation of MCL-1 Dependency Utilizing a Highly Selective Small Molecule Inhibitor.

Sample Metadata Fields

Cell line

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accession-icon GSE24558
GBM brain tumors
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Glioblastoma stem-like cells give rise to tumour endothelium.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE24557
Exon-level expression profiles of GBM brain tumors
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Transcriptome analysis of RNAs from brain tumor

Publication Title

Glioblastoma stem-like cells give rise to tumour endothelium.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE24244
Gene expression profiling of four subpopulations in GBM
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

GBM is a heterogenous brain tumor with hyperproliferation of endothelial cells. In order to understand the cellular mechanism of vasculogenesis in GBM, four fractions of cells are seperated. Microarray assays was performed to examine the potential lineage relationship and the signal pathways involved in determining the cell identity and function.

Publication Title

Glioblastoma stem-like cells give rise to tumour endothelium.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon SRP155027
RNA-seq of PC9 cells tolerant to gefitinib
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

EGFR inhibitors (EGFRi) are effective against EGFR mutant lung cancers. The efficacy of these drugs however is mitigated by the outgrowth of resistant cells, most often driven by a secondary acquired mutation in EGFR, T790M. We recently demonstrated that T790M can arise de novo during treatment (Hata et al., Nature Medicine 2016); it follows that one potential therapeutic strategy to thwart resistance would be identifying and eliminating these cells (referred to as drug tolerant cells (DTCs)) prior to acquiring secondary mutations like T790M. We have developed DTCs to EGFRi in EGFR mutant lung cancer cell lines. Subsequent analyses of DTCs included RNA-seq, high-content microscopy, and protein translational assays. Based on these results, we tested the ability of MCL-1 BH3 mimetics to combine with EGFR inhibitors to eliminate DTCs and shrink EGFR mutant lung cancer tumors in vivo. Overall design: The NSCLC cell line PC9 was made tolerant to gefitinib over 6-days. Replicates were performed at a minimum of duplicates. EGFR inhibitors (EGFRi) are effective against EGFR mutant lung cancers. The efficacy of these drugs however is mitigated by the outgrowth of resistant cells, most often driven by a secondary acquired mutation in EGFR, T790M. We recently demonstrated that T790M can arise de novo during treatment (Hata et al., Nature Medicine 2016); it follows that one potential therapeutic strategy to thwart resistance would be identifying and eliminating these cells (referred to as drug tolerant cells (DTCs)) prior to acquiring secondary mutations like T790M. We have developed DTCs to EGFRi in EGFR mutant lung cancer cell lines. Subsequent analyses of DTCs included RNA-seq, high-content microscopy, and protein translational assays. Based on these results, we tested the ability of MCL-1 BH3 mimetics to combine with EGFR inhibitors to eliminate DTCs and shrink EGFR mutant lung cancer tumors in vivo.

Publication Title

Increased Synthesis of MCL-1 Protein Underlies Initial Survival of <i>EGFR</i>-Mutant Lung Cancer to EGFR Inhibitors and Provides a Novel Drug Target.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE18027
BTG1 regulates glucocorticoid receptor autoinduction in acute lymphoblastic leukemia
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

RNAi mediated knockdown of BTG1 in the acute lymphoblastic cell line RS4;11 causes this cell line to become resistant to prednisolone treatment when compared to control cells.

Publication Title

BTG1 regulates glucocorticoid receptor autoinduction in acute lymphoblastic leukemia.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE7355
Candida-induced expression profile in HUVEC
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Using oligonucleotide microarray analysis, we identified 56 genes that were transcriptionally up-regulated and 69 that were suppressed upon exposure of endothelial cells to C. albicans. Among the regulated genes those attributed to the categories chemotaxis, signaling, and transcription and translation were remarkably overrepresented.

Publication Title

Candida albicans triggers activation of distinct signaling pathways to establish a proinflammatory gene expression program in primary human endothelial cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE35240
Gene expression in mitotic tissues of Drosophila larvae without centrosomes or too many centrosomes
  • organism-icon Drosophila melanogaster
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Centrosome defects are a common feature of many cancers. Surprisingly, flies can proceed through the majority of development without centrosomes or with amplified centrosomes in most of their cells. It is unclear whether this is because centrosome defects do not cause many problems in Drosophila cells, or because they can adapt to cope with any problems that arise. Indeed, centrosome loss and centrosome amplification predispose fly brain cells to form tumours. Here we assess how centrosome loss or centrosome amplification perturbs cell physiology by profiling the global transcriptome of Drosophila larval brains and imaginal discs that either lack centrosomes or have too many centrosomes.

Publication Title

Centrosome loss or amplification does not dramatically perturb global gene expression in Drosophila.

Sample Metadata Fields

Specimen part

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accession-icon GSE21511
EWS-FLI1 reactivates a neural crest stem cell program in human neural crest-derived mesenchymal stem cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Ewing sarcoma family of tumors (ESFT) are aggressive bone and soft tissue tumors of unknown cellular origin. Most ESFT express EWS-FLI1, a chimeric protein which functions as a growth-promoting oncogene in ESFT but is toxic to most normal cells. A major difficulty in understanding EWS-FLI1 function has been the lack of an adequate model in which to study EWS-FLI1-induced transformation. Although the cell of origin of ESFT remains elusive, both mesenchymal (MSC) and neural crest (NCSC) have been implicated. We recently developed the tools to generate NCSC from human embryonic stem cells (hNCSC). In the current study we used this model to test the hypothesis that neural crest-derived stem cells are the cells of origin of ESFT and to evaluate the consequences of EWS-FLI1 expression on human neural crest biology.

Publication Title

Modeling initiation of Ewing sarcoma in human neural crest cells.

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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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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