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accession-icon GSE17987
Novel treatment of human pancreatic cancer using masitinib combined with standard gemcitabine chemotherapy
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Masitinib is a tyrosine kinase inhibitor of c-Kit, PDGFR and , and to some extent Lyn of the Src kinase family. We evaluated the therapeutic potential of masitinib in vitro on human pancreatic tumour cell lines and in vivo in a mouse model of human pancreatic cancer.

Publication Title

Masitinib combined with standard gemcitabine chemotherapy: in vitro and in vivo studies in human pancreatic tumour cell lines and ectopic mouse model.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon SRP055475
A MYC-driven change in mitochondrial dynamics limits stem cell properties of mammary epithelial cells (RNA-seq)
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerIIx

Description

In several developmental lineages, an increase in expression of the MYC proto-oncogene drives the transition from quiescent stem cells to transit amplifying cells. The mechanism by which MYC restricts self-renewal of adult stem cells is unknown. Here, we show that MYC activates a stereotypic transcriptional program of genes involved in protein translation and mitochondrial biogenesis in mammary epithelial cells and indirectly inhibits the YAP/TAZ co-activators that are essential for mammary stem cell self-renewal. We identify a phospholipase of the mitochondrial outer membrane, PLD6, as the mediator of MYC activity. PLD6 mediates a change in the mitochondrial fusion/fission balance that promotes nuclear export of YAP/TAZ in a LATS- and RHO-independent manner. Mouse models and human pathological data confirm that MYC suppresses YAP/TAZ activity in mammary tumors. PLD6 is also required for glutaminolysis, arguing that MYC-dependent changes in mitochondrial dynamics balance cellular energy metabolism with the self-renewal potential of adult stem cells. Overall design: RNA-Seq Experiments in 2 different primary breast epithelial cell lines (HMLE, which were sorted according to CD44/CD24 surface markers & unsorted IMEC). Both cell lines expressed a doxycycline-inducible version of MYC. For the HMLE cell line DGE analysis was performed for the uninduced (EtOH) situation, comparing CD44high vs CD44 low and for the induced situation Dox vs. EtOH for the CD44high population. For the IMEC cell line DGE was performed by comparing Dox-treated populations expressing either Dox-inducible MYC or a vector control which allows to filter out potential effects due to doxycycline treatment.

Publication Title

A MYC-Driven Change in Mitochondrial Dynamics Limits YAP/TAZ Function in Mammary Epithelial Cells and Breast Cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE73416
Escherichia coli MG1655 gene expression in glucose minimum media
  • organism-icon Escherichia coli
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

M9 glucose minimum media were analyzed for RNA expression.

Publication Title

Codon influence on protein expression in E. coli correlates with mRNA levels.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE87164
Gene expression in MMTV-PyMT whole tumor, CD3+ lymphocytes or CD11b+ myeloid cells with and without Class IIa HDAC inhibitor treatment
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Class IIa HDAC inhibition reduces breast tumours and metastases through anti-tumour macrophages.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE76659
Differential gene expression in either CD3+ lymphocytes or CD11b+ myeloid cells due to Class IIa HDAC inhibitor treatment
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The aim of this study was to identify differential gene expression resulting from the inhibition of class IIa HDACs in the CD3+ or CD11b+ cells residing in MMTV-PyMT tumors.

Publication Title

Class IIa HDAC inhibition reduces breast tumours and metastases through anti-tumour macrophages.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE17385
Gene expression profiling from MM1.S cells with control or beta-catenin knockdown.
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

MM1.S cells stably transduced with control or b-catenin shRNA were established. Total RNA was isolated from 5x 10^6 cells of each in triplicate.

Publication Title

Aurora kinase A is a target of Wnt/beta-catenin involved in multiple myeloma disease progression.

Sample Metadata Fields

Cell line

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accession-icon GSE87163
MMTV-PyMT whole tumor gene expression with and without Class IIa HDAC inhibitor treatment
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The aim of this study was to identify differential gene expression resulting from the inhibition of class IIa HDACs in the CD3+ or CD11b+ cells residing in MMTV-PyMT tumors.

Publication Title

Class IIa HDAC inhibition reduces breast tumours and metastases through anti-tumour macrophages.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE37700
Reactivation of ERK signaling causes resistance to EGFR kinase inhibitors
  • organism-icon Homo sapiens
  • sample-icon 6 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

Reactivation of ERK signaling causes resistance to EGFR kinase inhibitors.

Sample Metadata Fields

Cell line

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accession-icon GSE37699
Aberrant ERK signaling causes resistance to EGFR kinase inhibitors
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

The clinical efficacy of EGFR kinase inhibitors is limited by the development of drug resistance. The irreversible EGFR kinase inhibitor WZ4002 is effective against the most common mechanism of drug resistance mediated by the EGFR T790M mutation. Here we show that in multiple complementary models harboring EGFR T790M, resistance to WZ4002 develops through aberrant activation of ERK signaling caused by either an amplification of MAPK1 or by downregulation of negative regulators of ERK signaling. Inhibition of MEK or ERK restores sensitivity to WZ4002, and the combination of WZ4002 and a MEK inhibitor prevents the emergence of drug resistance. The WZ4002 resistant MAPK1 amplified cells also demonstrate an increase both in EGFR internalization and a decrease in sensitivity to cytotoxic chemotherapy compared to the parental counterparts. Our findings provide insights into mechanisms of drug resistance to EGFR kinase inhibitors and highlight rational combination therapies that should be evaluated in clinical trials.

Publication Title

Reactivation of ERK signaling causes resistance to EGFR kinase inhibitors.

Sample Metadata Fields

Cell line

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accession-icon SRP154146
ABCA1 haplodeficiency affects the brain transcriptome following traumatic brain injury in mice expressing human APOE isoforms
  • organism-icon Mus musculus
  • sample-icon 58 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We examined the impact of Abca1 deficiency and APOE isoform expression on the response to TBI using 3-months-old, human APOE3+/+ (E3/Abca1+/+) and APOE4+/+ (E4/Abca1+/+) targeted replacement mice, and APOE3+/+ and APOE4+/+ mice with only one functional copy of the Abca1 gene (E3/Abca1+/-; E4/Abca1+/-). TBI-treated mice received a craniotomy followed by a controlled cortical impact (CCI) brain injury in the left hemisphere; sham-treated mice received the same surgical procedure without the impact. We performed RNA-seq using samples from cortices and hippocampi collected at 14 days post-injury, followed by genome-wide differential gene expression analysis. Overall design: We used 3-months-old, human APOE3+/+ (E3/Abca1+/+) and APOE4+/+ (E4/Abca1+/+) targeted replacement mice, and APOE3+/+ and APOE4+/+ mice with only one functional copy of the Abca1 gene (E3/Abca1+/-; E4/Abca1+/-). Groups consisted of 6-8 animals of both genders. TBI-treated mice received a craniotomy followed by a controlled cortical impact (CCI) brain injury in the left hemisphere; sham-treated mice received the same surgical procedure without the impact. We performed RNA-seq using samples from cortices and hippocampi collected at 14 days post-injury from 58 samples, followed by genome-wide differential gene expression analysis.

Publication Title

ABCA1 haplodeficiency affects the brain transcriptome following traumatic brain injury in mice expressing human APOE isoforms.

Sample Metadata Fields

Sex, Treatment, Subject

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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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