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Modulation of lymphangiogenesis: a new target for aspirin and other nonsteroidal anti-inflammatory agents? A systematic review.
J Clin Pharmacol. 2012 Nov;52(11):1749-54
Authors: Yiannakopoulou E
Abstract
Recent studies have implicated that lymphangiogenesis plays a role in the development of metastasis in experimental cancer models and in certain types of human tumors. Epidemiological and laboratory data suggest that non steroidal anti-inflammatory agents (NSAIDs) have antitumor activities, although the mechanisms have not been elucidated. This systematic review aimed to synthesize data on the effect of aspirin and other NSAIDs on lymphangiogenesis. In particular, an answer was attempted to be found for the following primary questions: Is there an effect of aspirin and NSAIDs on lymphangiogenesis? If yes, is this effect mediated through COX-II inhibition or through COX-II-independent mechanisms? Electronical databases were searched with the appropriate search terms for the period from 1966 up to and including February 2011. The few identified experimental trials indicated that aspirin and other NSAIDs inhibit lymphangiogenesis, with a potential decrease in metastatic spread, possibly through COX-II-dependent regulation of VEGF-C expression. COX-II-independent mechanisms of inhibition of lymphangiogenesis by salicylates and the other NSAIDs have not been investigated. Although further research validation is needed, this proposed effect of NSAIDs might have therapeutic implications in chemoprevention, adjuvant chemotherapy, and treatment of metastatic disease.
PMID: 22174438 [PubMed - indexed for MEDLINE]
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