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Cyclooxygenase-2 (COX-2)–Independent Anticarcinogenic Effects of Selective COX-2 Inhibitors

Grösch, Sabine, Maier, Thorsten Jürgen, Schiffmann, Susanne, Geisslinger, Gerd·2006·JNCI: Journal of the National Cancer Institute

Abstract

Nonsteroidal antiinflammatory drugs (NSAIDs) appear to reduce the risk of developing cancer. One mechanism through which NSAIDs act to reduce carcinogenesis is to inhibit the activity of cyclooxygenase-2 (COX-2), an enzyme that is overexpressed in various cancer tissues. Overexpression of COX-2 increases cell proliferation and inhibits apoptosis. However, selective COX-2 inhibitors can also act through COX-independent mechanisms. In this review, we describe the COX-2-independent molecular targets of these COX-2 inhibitors and discuss how these targets may be involved in the anticarcinogenic activities of these selective COX-2 inhibitors. We also compare the concentrations of these inhibitors used in in vitro and in vivo experiments and discuss the implications of the in vitro studies for clinical management of cancer with these drugs.

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Metadata

Authors
Grösch, S., Maier, T. J., Schiffmann, S., & Geisslinger, G.
Venue
JNCI: Journal of the National Cancer Institute
Published
2006-06-07
Volume
98
Issue
11
Pages
736-747
ISSN
  • 1460-2105
  • 0027-8874
Cited by
400
References
3
Language
en

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CoChat. (2026). Citation check: Cyclooxygenase-2 (COX-2)–Independent Anticarcinogenic Effects of Selective COX-2 Inhibitors. https://app.cochat.ai/papers/10.1093/jnci/djj206
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Grösch, S., Maier, T. J., Schiffmann, S., & Geisslinger, G. (2006). Cyclooxygenase-2 (COX-2)–Independent Anticarcinogenic Effects of Selective COX-2 Inhibitors. JNCI: Journal of the National Cancer Institute. https://doi.org/10.1093/jnci/djj206