Apoptosis primarily accounts for the growth-inhibitory properties of sulindac metabolites and involves a mechanism that is independent of cyclooxygenase inhibition, cell cycle arrest, and p53 induction. [electronic resource]
Producer: 19970715Description: 2452-9 p. digitalISSN:- 0008-5472
- 16,16-Dimethylprostaglandin E2 -- pharmacology
- Adenocarcinoma -- metabolism
- Anti-Inflammatory Agents, Non-Steroidal -- pharmacology
- Apoptosis -- drug effects
- Cell Cycle -- physiology
- Cell Division -- drug effects
- Cell Survival -- drug effects
- Colonic Neoplasms -- metabolism
- Cyclooxygenase Inhibitors -- metabolism
- Dose-Response Relationship, Drug
- Fluorouracil -- pharmacology
- Growth Inhibitors -- pharmacology
- Humans
- Prostaglandin-Endoperoxide Synthases -- metabolism
- Sulindac -- metabolism
- Time Factors
- Tumor Cells, Cultured
- Tumor Suppressor Protein p53 -- metabolism
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Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
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