(3S-5S-6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3-5-dihydroxyhept-6-enoic-acid has been researched along with Cell-Transformation--Neoplastic* in 2 studies
2 other study(ies) available for (3S-5S-6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3-5-dihydroxyhept-6-enoic-acid and Cell-Transformation--Neoplastic
| Article | Year |
|---|---|
Identifying chemopreventive agents for obesity-associated cancers using an efficient, 3D high-throughput transformation assay.
Obesity is associated with ~40% of cancer diagnoses but there are currently no effective preventive strategies, illustrating a need for chemoprevention. We previously demonstrated that fibroblast growth factor 2 (FGF2) from adipose tissue stimulates malignant transformation, as measured by growth in soft agar, the gold-standard in vitro transformation assay. Because the soft agar assay is unsuitable for high throughput screens (HTS), we developed a novel method using 3D growth in ultra-low attachment conditions as an alternative to growth in agar to discover compounds that inhibit transformation. Treating non-tumorigenic, skin epithelial JB6 P Topics: Animals; Antineoplastic Agents; Cell Culture Techniques; Cell Proliferation; Cell Transformation, Neoplastic; Drug Screening Assays, Antitumor; Fibroblast Growth Factor 2; Fibroblasts; Fluvastatin; High-Throughput Screening Assays; Humans; Mice; Models, Biological; Neoplasms; Obesity; Podophyllotoxin; Skin | 2019 |
Carcinogenicity and mutagenicity studies with fluvastatin, a new, entirely synthetic HMG-CoA reductase inhibitor.
The HMG-CoA reductase inhibitors are a new and novel class of cholesterol-lowering agents which are widely used worldwide. Fluvastatin is the first entirely synthetic compound in this class and is structurally distinct from fungal metabolite derivatives which are already marketed. As the liver is the site of some toxic effects for these compounds, it was not entirely unexpected that liver cancer was found in rats and/or mice with the first three marketed compounds, lovastatin, pravastatin, and simvastatin. Four lifetime carcinogenicity studies (two rat and two mouse) did not give any evidence that fluvastatin induced liver tumors in rodents. Fluvastatin induced thyroid neoplasms in rats and forestomach papillomas in rodents, as other compounds in this pharmacologic class have also done. The genotoxic potential of fluvastatin has been assessed in vitro using Salmonella typhimurium, Escherichia coli (gene mutations), V79 Chinese hamster cells (HGPRT gene mutations, chromosomal aberrations), rat hepatocyte primary cultures (DNA repair), and BALB/3T3 cells (malignant transformations). Fluvastatin was also tested in vivo for clastogenicity using the mouse bone marrow micronucleus test and by performing a cytogenetic analysis in the rat bone marrow after acute and subacute treatment. In all seven assays fluvastatin was found to be free of any genotoxic potential. Topics: 3T3 Cells; Animals; Anticholesteremic Agents; Bacteria; Carcinogenicity Tests; Carcinogens; Cell Transformation, Neoplastic; Cells, Cultured; Cricetinae; Cricetulus; Cytogenetics; DNA Repair; Fatty Acids, Monounsaturated; Female; Fluvastatin; Indoles; Male; Mice; Mice, Inbred Strains; Micronucleus Tests; Mutagenicity Tests; Mutagens; Rats; Rats, Inbred Strains | 1994 |