作者: Linda C. Hsi , Thomas E. Eling
DOI: 10.1007/978-1-59259-302-6_15
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摘要: Nonsteroidal anti-inflammatory drugs (NSAIDS) are promising agents for cancer chemoprevention, likely owing to their ability inhibit prostaglandin (PG) biosynthesis, particularly biosynthesis dependent upon the inducible proinflammatory enzyme cyclooxygenase-2 (COX-2). Overexpression of COX-2 resulting in excessive PG production has been observed early stages carcinogenesis and seems be a consistent feature neoplastic development wide variety tissues. The mechanism overexpression is not clear, but may occur along signaling pathways inflammation tissue repair that become activated course tumor promotion. PGs formed dysregulated COX pathway appear mediate promotion animal models play role processes involved growth such as angiogenesis, apoptosis, immunosupression.