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| Title / Description | Lovastatin effect on breast tumors in HER2/neu transgenic mice |
| Accession | GSE42787 |
| Summary | The statins are a family of inhibitors of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase enzyme, which converts acetyl-CoA into mevalonic acid. Since HMG-CoA reductase catalyzes the rate-limiting step in the mevalonate pathway of cholesterol biosynthesis, it was thought that the major clinical benefit of statins was to reduce cholesterol levels in the bloodstream; statins are thus in wide clinical use for the prevention and treatment of cardiovascular disease. Nonetheless, mevalonate is also the precursor of isoprenoid compounds, which are substrates for the post-translational modification of many proteins involved in cell signaling. The blockade of isoprenoid synthesis might explain the pleiotropic effects described for statins in extrahepatic tissues, including inhibition of pathogen infection and anti-inflammatory and immunomodulatory activities. We used microarrays to find differentially expressed genes in spontaneous breast tumors from mice treated with lovastatin (Lov) or vehicle (ethanol) as control. |
| Organism | Mus musculus |
| Platform | GPL1261 |
| Normalized | False |
| Parsed SOFT file |
| Differential expression method | Characteristic Direction |
| Cutoff | 500 |
| Cell_type | Breast |
| Drug_id | DB00227 |
| Drug_name | Lovastatin |
| Organism | Mouse |
| Principal Component Analysis | |
| Hierarchical clustering |
| Gene lists | Enrichr | L1000CDS2 | PAEA | Crowdsourcing | |
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