Prostaglandins and cancer.
Journal: 2006/January - Gut
ISSN: 0017-5749
Abstract:
Chemoprevention has been considered as a possible approach for cancer prevention. A significant effort has been made in the development of novel drugs for both cancer prevention and treatment over the past decade. Recent epidemiological studies and clinical trials indicate that long term use of aspirin and similar agents, also called non-steroidal anti-inflammatory drugs (NSAIDs), can decrease the incidence of certain malignancies, including colorectal, oesophageal, breast, lung, and bladder cancers. The best known targets of NSAIDs are cyclooxygenase (COX) enzymes, which convert arachidonic acid to prostaglandins (PGs) and thromboxane. COX-2 derived prostaglandin E(2)(PGE(2)) can promote tumour growth by binding its receptors and activating signalling pathways which control cell proliferation, migration, apoptosis, and/or angiogenesis. However, the prolonged use of high dosages of COX-2 selective inhibitors (COXIBs) is associated with unacceptable cardiovascular side effects. Thus it is crucial to develop more effective chemopreventive agents with minimal toxicity. Recent efforts to identify the molecular mechanisms by which PGE(2) promotes tumour growth and metastasis may provide opportunities for the development of safer strategies for cancer prevention and treatment.
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Gut 55(1): 115-122

Prostaglandins and cancer

D Wang, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA
R N DuBois, Departments of Medicine, Cancer Biology, and Cell and Developmental Biology, Vanderbilt University Medical Center, Nashville, TN, USA, and The Vanderbilt‐Ingram Cancer Center, Nashville, TN, USA
Correspondence to: Professor R N DuBois
The Vanderbilt‐Ingram Cancer Center, Room 698, Preston Research Building, 2300 Pierce Ave, Nashville, Tennessee 37232‐6838, USA; raymond.dubois@vanderbilt.edu
D Wang, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USAR N DuBois, Departments of Medicine, Cancer Biology, and Cell and Developmental Biology, Vanderbilt University Medical Center, Nashville, TN, USA, and The Vanderbilt‐Ingram Cancer Center, Nashville, TN, USACorrespondence to: Professor R N DuBois
The Vanderbilt‐Ingram Cancer Center, Room 698, Preston Research Building, 2300 Pierce Ave, Nashville, Tennessee 37232‐6838, USA; raymond.dubois@vanderbilt.edu
Keywords: cyclooxygenase, prostaglandins, non‐steroidal anti‐inflammatory drugs, cancer, inflammation

Acknowledgements

We acknowledge support from the United States Public Health Services Grants RO1‐DK‐62112 and PO1‐CA77839. RND is the Hortense B Ingram Professor of Molecular Oncology and the recipient of an NIH MERIT award (R37‐DK47297). We also thank the TJ Martell Foundation and the National Colorectal Cancer Research Alliance (NCCRA) for generous support.

Acknowledgements

Footnotes

Conflict of interest: None declared.

Footnotes

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