Project description:Analysis of the effects of targeting NOS2 at the gene expression level. Our studies demonstrated a role for NOS2 in glioma biology through the maintenance of the glioma stem cell phenotype. Microarray results provide novel targets of NOS2 and suggest mechanisms through which NOS2 contributes to glioma stem cell biology. Glioma stem cells isolated from two different human glioma xenografts were infected with a non-targeting control shRNA or two different shRNAs directed against NOS2 (each treatment in each tumor performed in technical duplicates).

2011-07-08 | E-GEOD-29750 | biostudies-arrayexpress

Glioma MYC gene signature

Project description:There is little overlap on publicily avaiable gene signatures and it is unclear how relevant these are to glioma biology. MYC is a very dynamically regulated gene, and it's gene signature will vary with respect to cell context. To determine what genes fall within the MYC signature of glioma, we performed ChIP-SEQ upon 4 different glioma PDX with two different MYC antibodies. The overlapping enriched genes will provide context of a MYC signature within the context of glioma.

2022-09-12 | GSE206873 | GEO

Inherited functional regulatory risk variants for common human cancers

Project description:Single nucleotide variants (SNVs) in regulatory DNA are linked to inherited cancer risk. Massively parallel reporter assays (MPRA) of 5,031 SNVs linked to 14 neoplasms comprising >90% of human malignancies were performed in pertinent diploid cell types then integrated with matching chromatin accessibility, looping, and eQTL data to identify 411 regulatory SNVs and their putative target eGenes. The latter highlighted specific protein networks in lifetime cancer risk, including mitochondrial translation, proliferation, signaling, adhesion, and immunity. This cancer SNV compendium underscores the importance of studying pathogenic variants in disease-relevant cells and implicates specific dysregulated gene networks in cancer predisposition. It also indicates that inherited cancer risk can impact the same gene via orthogonal genetic mechanisms of dysregulated expression as well as protein coding sequence alteration and demonstrates that a subset of germline-encoded risk genes also enable tumor growth of established cancers.

2024-08-22 | GSE183348 | GEO

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