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Titlebook: COX-2 Blockade in Cancer Prevention and Therapy; Randall E. Harris Book 2003 Springer Science+Business Media New York 2003 Prevention of b

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Cyclooxygenase-1 and Cyclooxygenase-2 Knockout Mice Provide Insights into Beneficial and Adverse Efftaglandins (PGs), i.e., PGE., PGD., PGI., PGF., and thromboxane A2 . Both isoforms are biological targets for the widely used class of medicines known as nonsteroidal anti-inflammatory drugs (NSAIDs); and NSAIDs are believed to cause their biological effects by effectively reducing PG production. Ho
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Cyclooxygenase-2, Prostaglandins, and Colorectal Carcinogenesiso approx 550,00 annual deaths worldwide. This failure in treatment has led to a search for novel, nontoxic agents that could possibly be utilized to prevent the development of the disease. Recently, inhibitors of the cyclooxygenase-2 (COX-2) enzyme have emerged as a class of drugs that may represent
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Cyclooxygenase-2 and CancerX-2 involvement in transformation, maintenance of tumor growth, viability, and metastasis. Included are descriptions of the chronic upregulation of COX-2 in multiple human tumors, as well as the pharmacological evidence of the anti-angiogenic activity of COX-2 inhibitors in animal models. Collective
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Interactions of Cyclooxygenase and Aromatase Pathways in Normal and Malignant Breast Cells 40,800 women in the United States will die from breast cancer in 2001. Currently, one out of eight American women will develop breast cancer in her lifetime (1). The rate of breast cancer incidence has increased 2–3% per year over the past decade in both premenopausal and postmenopausal women.
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https://doi.org/10.1007/978-94-009-2255-6pment of several human cancers. Specifically, polyunsaturated fatty acids such as linoleic acid (C18:2,n-6) and arachidonic acid (C20:4,n-6) enhance experimental carcinogenesis, tumor development, and tumor progression. In contrast, monounsaturated fatty acids such as oleic acid (C18:1, n-9) or poly
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