Snowmass, Co. (September 13, 2004) Over at least the last decade it has been recognized that the growth of new blood vessels is critical in the pathogenesis of cancer because it increases blood supply to malignant tissue. Relatively recently, a novel pathogenic role of angiogenesis has been established for such chronic inflammatory diseases as rheumatoid arthritis, psoriasis and atherosclerosis.

As a result, suppressing neoangiogenesis is being investigated as a therapeutic approach for not only cancer, but also chronic inflammation.

Whether neoangiogenesis also occurs in Crohn's Disease (CD) and ulcerative colitis (UC), the major constituents of Inflammatory Bowel Diseases (IBD), has never been studied, according to the authors of a paper presented at an IBD translational conference sponsored by the American Physiological Society.

The paper is entitled, "Neoangiogenesis: a new component in Inflammatory Bowel Diseases pathogenesis."

Lead author Silvio Danese of Case Western Reserve University School of Medicine and Universita' Cattolica del S. Cuore, Rome, Italy, collaborated with colleagues Miquel Sans, Brenda Reyes-Rivera, Gail West, Homa Phillips, Joe Willis and Claudio Fiocchi at Case Western Reserve University School of Medicine; Carol de la Motte at the Cleveland Clinic Foundation; and Roberto Pola and Antonio Gasbarrini at Universita' Cattolica del S. Cuore.

According to Danese, "Our results show that increased vascularization is present in IBD, and the inflamed mucosal microenvironment actively promotes angiogenesis." Furthermore, he said that "the intestinal microvascularization of both CD and UC displays an activated profile as shown by the expression of angiogenic marker V3 integrin.

"Targeting this integrin could be a potential therapeutic approach for IBD," similar to approaches in other forms of chronic inflammation, Danese said. "These r
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13-Sep-2004

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