We utilized whole genome sequencing of mRNA (RNA-seq) to understand the extent to which the senescence-associated secretory phenotype is regulated by p38MAPK Overall design: Examination of replicates of young, senescent or p38MAPK-inhibited senescent BJ human foreskin fibroblasts.
p38MAPK plays a crucial role in stromal-mediated tumorigenesis.
No sample metadata fields
View SamplesMouse skin fibroblasts (MSFs) were obtained from a FASST (Fibroblasts Accelerate Stromal-Supported Tumorigenesis) mouse. This mouse model allows for spatial and temporal control for senescence induction by using a stromal specific Cre-recombinase driven by the pro-collagen-alpha II promoter. The stromal specific Cre activates expression of the p27IRESGFP transgene that is expressed from the ROSA locus. We cultured the MSFs in vitro, induced senescence using 10uM tamoxifen added to the media. Non-senescent cells were treated with equal volume of vehicle alone (ethanol). Upon tamoxifen treatment, cells were moved to a modular incubation chamber and maintained at 3% oxygen at 37 degrees celcius for 12 days total before collection. At the time of collection, cells were trypsynized and pelleted by centrifugation. The cells were lysed using Trysol reagent and RNA was isolated using a RiboPure RNA isolation kit (Ambion). Overall design: For this study, 2 treatment groups were analyzed (non-senescent, EtOH samples and senescent, TAM samples). Each treatment group was performed 3 times for a total of 6 samples for analysis. The gene expression analysis is a comparison of expression in senescent (TAM) vs non-senescent (EtOH) mouse skin fibroblasts.
Stromal senescence establishes an immunosuppressive microenvironment that drives tumorigenesis.
Specimen part, Cell line, Treatment, Subject
View SamplesWe used microarrays to detail the global programme of gene expression in embryonic stem cells, early differentiated embrioid bodies and effect of short-term ATRA treatment.
Activation of retinoic acid receptor signaling coordinates lineage commitment of spontaneously differentiating mouse embryonic stem cells in embryoid bodies.
Cell line
View SamplesThe goal of this study was to determine if blood circulating monocytes of metastatic breast cancer patient would express a different activation profile compared to healthy donors, in order to use this specific changesas biomarkers to monitor then response to therapy Overall design: CD11b+ cells were extracted from all blood of 4 healthy donors and 4 metastatic breast cancer patients using magnetic beads separation (Miltenyi). CD11b+ cells were then lysed and mRNA was extracted to perform RNASeq.
Bevacizumab specifically decreases elevated levels of circulating KIT+CD11b+ cells and IL-10 in metastatic breast cancer patients.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Therapeutic targeting of the MYC signal by inhibition of histone chaperone FACT in neuroblastoma.
Age, Specimen part, Cell line, Treatment
View SamplesAmplification of the MYCN oncogene predicts treatment resistance in childhood neuroblastoma. Using a MYC target gene signature that predicts poor neuroblastoma prognosis we identified the histone chaperone, FAcilitates Chromatin Transcription (FACT), as a crucial mediator of the MYC signal and a therapeutic target in the disease. FACT and MYCN expression created a forward feedback loop in neuroblastoma cells that was essential for maintaining mutual high expression. FACT inhibition by the small molecule Curaxin compound, CBL0137, markedly reduced tumor initiation and progression in vivo. CBL0137 exhibited strong synergy with chemotherapy in standard use by blocking repair of DNA damage caused by genotoxic drugs, thus creating a synthetic lethal environment in MYCN amplified neuroblastoma cells and a treatment strategy for MYCN-driven neuroblastoma
Therapeutic targeting of the MYC signal by inhibition of histone chaperone FACT in neuroblastoma.
Cell line, Treatment
View SamplesAmplification of the MYCN oncogene predicts treatment resistance in childhood neuroblastoma. Using a MYC target gene signature that predicts poor neuroblastoma prognosis we identified the histone chaperone, FAcilitates Chromatin Transcription (FACT), as a crucial mediator of the MYC signal and a therapeutic target in the disease. FACT and MYCN expression created a forward feedback loop in neuroblastoma cells that was essential for maintaining mutual high expression. FACT inhibition by the small molecule Curaxin compound, CBL0137, markedly reduced tumor initiation and progression in vivo. CBL0137 exhibited strong synergy with chemotherapy in standard use by blocking repair of DNA damage caused by genotoxic drugs, thus creating a synthetic lethal environment in MYCN amplified neuroblastoma cells and a treatment strategy for MYCN-driven neuroblastoma
Therapeutic targeting of the MYC signal by inhibition of histone chaperone FACT in neuroblastoma.
Cell line, Treatment
View SamplesWe measured gene expression of D. melanogaster female heads and abdomens after mating with males from six populations evolved under either enforced monogamy (no male-male competition, 3 populations) or sustained polygamy (intense male-male competition, 3 populations). Overall design: Three samples of virgin female heads and six samples of mated female heads (one each per male evolved population, of which there are three monogamous and three polygamous), for nine libraries. Also, three samples of virgin female abdomens and six samples of mated female abdomens (one each per male evolved population, of which there are three monogamous and three polygamous), for nine libraries. In total, eighteen libraries sequenced in 8 lanes.
Sexual conflict drives male manipulation of female postmating responses in <i>Drosophila melanogaster</i>.
Sex, Specimen part, Subject
View SamplesAutosomal recessive polycystic kidney disease is a severe, monogenetically inherited kidney and liver disease and PCK rats carrying the orthologous mutant gene serve as a model of human disease. We combined selective MALDI imaging of sulfated kidney lipids and Fisher discriminant analysis of imaging data sets for identification of candidate lipid markers of progressive disease in PCK rats. Our study highlights strong increases in lower mass lipids as main classifiers of cystic disease. Structure determination by high resolution mass spectrometry identifies these altered lipids as taurine-conjugated bile acids. Beside increased levels of serum-cholesterol these sulfated lipids are selectively elevated in the PCK rat model but not in models of related hepatorenal fibrocystic diseases suggesting that they be molecular markers of the disease.
MALDI imaging MS reveals candidate lipid markers of polycystic kidney disease.
Sex, Age, Specimen part, Disease, Disease stage
View SamplesThe mammalian gastrointestinal tract harbors thousands of bacterial species that include symbionts as well as potential pathogens. The immune responses that limit access of these bacteria to underlying tissue remain poorly defined.
Gammadelta intraepithelial lymphocytes are essential mediators of host-microbial homeostasis at the intestinal mucosal surface.
Specimen part
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