Differentially expressed genes along the paraxial mesoderm of 12 somite stage zebrafish embryos are identified
Spatiotemporal compartmentalization of key physiological processes during muscle precursor differentiation.
Specimen part
View SamplesTo identify the potential ovarian cancer stem cell gene expression profile from isolated side population of fresh ascites obtained from women with high-grade advanced stage papillary serous ovarian adenocarcinoma
Identification of a potential ovarian cancer stem cell gene expression profile from advanced stage papillary serous ovarian cancer.
Specimen part
View SamplesTo identify a prognostic gene signature accounting for the distinct clinical outcomes in ovarian cancer patients
A gene signature predicting for survival in suboptimally debulked patients with ovarian cancer.
Specimen part
View SamplesThe HMG-box factor Tcf1 is required during T-cell development in the thymus and mediates the nuclear response to Wnt signals. Tcf1/ mice have previously been characterized and show developmental blocks at the CD4CD8 double negative (DN) to CD4+CD8+ double positive transition. Due to the blocks in T-cell development, Tcf1/ mice normally have a very small thymus. Unexpectedly, a large proportion of Tcf1/ mice spontaneously develop thymic lymphomas with 50% of mice developing a thymic lymphoma/leukemia at the age of 16 wk. These lymphomas are clonal, highly metastatic, and paradoxically show high Wnt signaling when crossed with Wnt reporter mice and have high expression of Wnt target genes Lef1 and Axin2. In wild-type thymocytes, Tcf1 is higher expressed than Lef1, with a predominance of Wnt inhibitory isoforms. Loss of Tcf1 as repressor of Lef1 leads to high Wnt activity and is the initiating event in lymphoma development, which is exacerbated by activating Notch1 mutations. Thus, Notch1 and loss of Tcf1 functionally act as collaborating oncogenic events. Tcf1 deficiency predisposes to the development of thymic lymphomas by ectopic up-regulation of Lef1 due to lack of Tcf1 repressive isoforms and frequently by cooperating activating mutations in Notch1. Tcf1 therefore functions as a T-cellspecific tumor suppressor gene, besides its established role as a Wnt responsive transcription factor. Thus, Tcf1 acts as a molecular switch between proliferative and repressive signals during T-lymphocyte development in the thymus.
The nuclear effector of Wnt-signaling, Tcf1, functions as a T-cell-specific tumor suppressor for development of lymphomas.
Specimen part
View SamplesChildhood T-ALL samples were compared with thymocyte subsets
Deregulated WNT signaling in childhood T-cell acute lymphoblastic leukemia.
Specimen part
View SamplesPurpose: The intergration of genetic and chemical screens identified SETD8 as a new druggable target in neuroblastoma tumor. The goal of this study is to evaluate the transcriptome profiling (RNA-seq) of Neuroblastoma cell lines after genetic and pharmacological inhibition of SETD8. Methods: mRNA profiles of NB cells after genetic and pharmacological inhibition of SETD8 were generated by deep sequencing in duplicate with Ilumina HiSeq2500 using Illumina TruSeq V4. The sequence reads were analyzed with software Trimmomatic, STAR and edgeR to determine the differetially expressed genes. qRT–PCR validation was performed using SYBR Green assays. Results: About 60 million sequence reads per sample were mapped to the human genome (hg19). Approximately 10% of the transcripts showed differential expression between the control and the treated samples, with a fold change =1.5 and p value <0.05. Altered expression of 12 genes was confirmed with qRT–PCR, demonstrating the high degree of sensitivity of the RNA-seq method. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to SETD8 function. Conclusions: Our study identifies SETD8 as a new therapeutic target in Neuroblastoma tumor. RNA-seq transcriptome analyses and functional studies revealed that SETD8 ablation rescued the proapoptotic and cell-cycle arrest functions of p53 through reactivation of the p53 canonical pathway by decreasing p53k382me1. Overall design: mRNA profiles of Neuroblastoma cells after genetic and pharmacological inhibition of SETD8 were generated by deep sequencing in duplicate with Ilumina HiSeq2500 using Illumina TruSeq V4.
Epigenetic siRNA and Chemical Screens Identify SETD8 Inhibition as a Therapeutic Strategy for p53 Activation in High-Risk Neuroblastoma.
Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A gene signature predictive for outcome in advanced ovarian cancer identifies a survival factor: microfibril-associated glycoprotein 2.
Specimen part, Disease stage, Cell line, Treatment
View SamplesTo demonstrate the use of a whole-genome oligonucleotide array to perform expression profiling on a series of microdissected late-stage, high-grade papillary serous ovarian adenocarcinomas to establish a prognostic gene signature correlating with survival and to identify novel survival factors in ovarian cancer.
A gene signature predictive for outcome in advanced ovarian cancer identifies a survival factor: microfibril-associated glycoprotein 2.
Specimen part, Disease stage
View SamplesTo identify the gene signature accounting for the distinct clinical outcomes in ovarian clear cell cancer patients
Identification of novel therapeutic targets in microdissected clear cell ovarian cancers.
Specimen part
View SamplesIdentification of signaling events contributing to the effect of recombinant MAGP2 on HUVECs and OVCA429. We used microarrays to identify the signaling events and up-regulated genes associated with MAGP2.
A gene signature predictive for outcome in advanced ovarian cancer identifies a survival factor: microfibril-associated glycoprotein 2.
Cell line, Treatment
View Samples