Ectopic Myc Expression in P493-6 B-cells at three levels:
Induction of ectopic Myc target gene JAG2 augments hypoxic growth and tumorigenesis in a human B-cell model.
Specimen part, Cell line
View SamplesGene expression in response to changes in sulfur supply was studied in P. aeruginosa E601, a cystic fibrosis isolate that displays mucin sulfatase activity, and in P. aeruginosa PAO1. A large family of genes was found to be upregulated by sulfate limitation in both isolates, encoding sulfatases and sulfonatases, transport systems, oxidative stress proteins, and a sulfate-regulated TonB/ExbBD complex. These genes were localized in five distinct islands on the genome, and encoded proteins with a significantly reduced content of cysteine and methionine. Growth of P. aeruginosa E601 with mucin as sulfur source led to a sulfate starvation response, but also to induction of genes involved with type III secretion systems.
Transcriptomic analysis of the sulfate starvation response of Pseudomonas aeruginosa.
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View SamplesHere we studied the epigenetic regulation of the naïve CD4+ T-cell activation response among children with IgE-mediated food allergy. Using integrated DNA methylation and transcriptomic profiling, we found that food allergy in infancy is associated with dysregulation of T-cell activation genes. Reduced expression of cell cycle related targets of the E2F and MYC transcription factor networks, and remodeling of DNA methylation at metabolic (RPTOR, PIK3D, MAPK1, FOXO1) and inflammatory genes (IL1R, IL18RAP, CD82) were associated with poorer T-lymphoproliferative responses in infancy after polyclonal activation of the T-cell receptor. Overall design: mRNA sequencing of naïve CD4+ T-cells under two conditions (anti-CD3+CD28 activated, or quiescent) at two ages (baseline (12months) and followup (2 or 4 years)) in allergic and non-allergic children.
Epigenetic dysregulation of naive CD4+ T-cell activation genes in childhood food allergy.
Sex, Subject
View SamplesLung cancer is a highly malignant tumor and the majority of cancer-related deaths are due to metastasis. The tumor microenvironment (TME) plays a fundamental role in the metastatic spread of tumor cells. Among other stromal cells, mesenchymal stem cells (MSCs) are known to be present within the TME and to be involved in cancer progression. However the majority of previous studies have been performed on bone marrow-derived MSCs. To investigate the role of the TME on the pulmonary MSC phenotype, we compared the expression profile of paired MSCs isolated from lung tumor (T-) and normal adjacent tissues (N-) from lung carcinoma patients.
Reciprocal modulation of mesenchymal stem cells and tumor cells promotes lung cancer metastasis.
Specimen part, Disease stage, Subject
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