Cyclooxygenase-2 and cancer treatment: Understanding the risk should be worth the reward

David G. Menter, Richard L. Schilsky, Raymond N. DuBois

Research output: Contribution to journalReview article

132 Scopus citations

Abstract

Targeting the prostaglandin (PG) pathway is potentially a critical intervention for the prevention and treatment of cancer. Central to PG biosynthesis are two isoforms of cyclooxygenase (COX 1 and 2), which produce prostaglandin H2 (PGH2) from plasma membrane stores of fatty acids. COX-1 is constitutively expressed, whereas COX-2 is an inducible isoform upregulated in many cancers. Differences between COX-1 and COX-2 catalytic sites enabled development of selective inhibitors. Downstream of the COX enzymes, prostaglandin E2 synthase converts available PGH 2 to prostaglandin E2 (PGE2), which can stimulate cancer progression. Significant research efforts are helping identify more selective targets and fully elucidate the downstream targets of prostaglandin E2-mediated oncogenesis. Nonetheless, as a key ratelimiting control point of PG biosynthesis, COX-2 continues to be an important anticancer target. As we embark upon a new era of individualized medicine, a better understanding of the individual risk and/or benefit involved in COX-2 selective targeting is rapidly evolving. This review endeavors to summarize developments in our understanding of COX-2 and its downstream targets as vital areas of anticancer research and to provide the current status of an exciting aspect of molecular medicine.

Original languageEnglish (US)
Pages (from-to)1384-1390
Number of pages7
JournalClinical Cancer Research
Volume16
Issue number5
DOIs
StatePublished - Mar 1 2010
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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