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1 Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, NIH, Bethesda, Maryland and 2 Kojin Hospital, Nagoya, Japan
Requests for reprints: J. Silvio Gutkind, Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, NIH, Building 30, Room 211, Bethesda, MD 20892-4340. Phone: 301-496-6259; Fax: 301-402-0823; E-mail: sg39v{at}nih.gov.
Colorectal cancer poses a major clinical challenge in the developed world where this disease is common. Recent findings suggest that the prostaglandin E2, the proinflammatory product of elevated cyclooxygenase-2 activity in colon cancer, stimulates cancer cell growth through a G proteindependent signaling pathway coupling the prostaglandin EP2 receptor to ß-catenin control. These findings provide new insights into the molecular framework needed to evaluate chemopreventive strategies for colorectal cancer. (Cancer Res 2006; 66(23): 11085-8)
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