The ability to dissect heterogeneity in colorectal cancer (CRC) is a critical step in developing predictive biomarkers. The goal of this study was to develop a gene expression based molecular subgrouping model, which predicts the likelihood that patients will respond to specific therapies.
Activation of the mTOR Pathway by Oxaliplatin in the Treatment of Colorectal Cancer Liver Metastasis.
No sample metadata fields
View SamplesComparison of R1 embryonic stem cells response to DMSO and retinoic acid and control
Meta-analysis of differentiating mouse embryonic stem cell gene expression kinetics reveals early change of a small gene set.
Specimen part, Cell line, Compound
View SamplesAdipose stroma in the mouse mammary gland undergoes remodeling throughout the 5 stages of development. These include nulliparous (virgin;never been pregnant), pregnant, lactating, involuting and regressed.
Pregnancy-associated breast cancers are driven by differences in adipose stromal cells present during lactation.
Specimen part
View SamplesGene knockdown of PBK led to decreased proliferation and sphere formation in the GSC cultures. Treatment of cells with different concentrations of HI-TOPK-032 almost completely abolished growth and proliferation and elicited a large increase in apoptosis
Targeting PBK/TOPK decreases growth and survival of glioma initiating cells in vitro and attenuates tumor growth in vivo.
Specimen part, Cell line
View SamplesDrosophila S2 cells treated with either GFP or spottes-dick dsRNA and incubated for 5 days. There are three replicates for each condition.
Spotted-dick, a zinc-finger protein of Drosophila required for expression of Orc4 and S phase.
No sample metadata fields
View SamplesTargeted molecular therapy has yielded remarkable outcomes in certain cancers, but specific therapeutic targets remain elusive for many others. As a result of two independent RNA interference (RNAi) screens, we identified pathway dependence on a member of the JAK tyrosine kinase family, TYK2, and its downstream effector STAT1 in T-cell acute lymphoblastic leukemia (T-ALL). Gene knockdown experiments consistently demonstrated TYK2 dependence in both T-ALL primary specimens and cell lines, and a small-molecule inhibitor of JAK kinase activity induced T-ALL cell death. Activation of this TYK2-STAT1 pathway in T-ALL cell lines occurs by gain-of-function TYK2 mutations or activation of IL-10 receptor signaling, and this pathway mediates T-ALL cell survival through upregulation of the anti-apoptotic protein BCL2. These findings indicate that in many T-ALL cases, the leukemic cells are dependent upon the TYK2-STAT1-BCL2 pathway for continued survival, supporting the development of molecular therapies targeting TYK2 and other components of this pathway.
TYK2-STAT1-BCL2 pathway dependence in T-cell acute lymphoblastic leukemia.
Specimen part, Cell line
View SamplesPurpose: Identify differentially expressed genes in placental samples from early-onset (EO) IUGR, EO-PE, as well as pregnancies complicated by both EO-PE and EO-IUGR Overall design: Methods: Isolated total RNA from human placenta at birth and used it for RNA-sequencing on the Hiseq2000. Sequences were aligned to the human transcriptome (hg19/genome_build37) . Aligned sequences were then used to obtain abundance measurements and conduct differential expression analysis.
Placental microRNAs in pregnancies with early onset intrauterine growth restriction and preeclampsia: potential impact on gene expression and pathophysiology.
Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Alignment of time course gene expression data and the classification of developmentally driven genes with hidden Markov models.
No sample metadata fields
View SamplesWe studied intragraft gene expression profiles of positive crossmatch (+XM) kidney transplant recipients who develop transplant glomerulopathy (TG) and those who do not. Whole genome microarray analysis and quantitative rt-PCR for 30 transcripts were performed on RNA from protocol renal allograft biopsies in 3 groups: 1) +XM/TG+ biopsies before and after TG; 2) +XM/NoTG; and 3) negative crossmatch kidney transplants (control). Microarray comparisons showed few differentially expressed genes between paired biopsies from +XM/TG+ recipients before and after the diagnosis of TG. Comparing +XM/TG+ and control groups, significantly altered expression was seen for 2,447 genes (18%) and 3,200 genes (24%) at early and late time points, respectively. Canonical pathway analyses of differentially expressed genes showed inflammatory genes associated with innate and adaptive immune responses. Comparing +XM/TG+ and +XM/NoTG groups, 3,718 probe sets were differentially expressed but these were over-represented in only 4 pathways. A classic accommodation phenotype was not identified. Using rt-PCR, the expression of inflammatory genes was significantly increased in +XM/TG+ recipients compared to control biopsies and to +XM/NoTG biopsies. In conclusion, pre-transplant DSA results in a gene expression profile characterized by inflammation and cellular infiltration and the majority of XM+ grafts are exposed to chronic injury.
Intragraft gene expression in positive crossmatch kidney allografts: ongoing inflammation mediates chronic antibody-mediated injury.
Specimen part, Time
View SamplesChanges in gene expression during berry development during a grape growing season were analysed.
Alignment of time course gene expression data and the classification of developmentally driven genes with hidden Markov models.
No sample metadata fields
View Samples