Study results from Emory University, Medical Department in the area of colon cancer published
2009 JUN 22 - (NewsRx.com) -- According to recent research published in the journal Gastroenterology, "Chronic inflammation is a risk factor for colon cancer (CC). Lysophosphatidic acid (LPA), a naturally produced phospholipid, mediates multiple effects that are vital to disease process, including inflammation and cancer." "The expression of LPA receptor 2 (LPA(2)) is up-regulated in several types of cancer, including ovarian and colon cancer, but the importance of LPA and LPA(2) in the development and progression of CC is unclear. In this study, we sought to determine whether LPA and LPA(2) regulate the progression of CC in vivo. We examined the potential role of LPA in CC progression by administering LPA to mice heterozygous for the adenomatous polyposis coli (Apc) allele. We determined the loss of LPA(2) function in tumorigenesis in the colon by treating mice with genetic deletion of LPA(2) (LPA(2)(-/-)) with azoxymethane and dextran sulfate sodium. We found that LPA increased tumor incidence in Apc(min/+) mice. LPA(2)(-/-) mice showed reduced mucosal damage and fewer tumors than wild-type (WT) mice. Reduced epithelial cell proliferation and decreases in beta-catenin, Kruppel-like factor 5, and cyclooxygenase-2 expression were observed in LPA(2)(-/-) mice. Unlike WT mice, induction of monocyte chemoattractant protein-1 and macrophage migration inhibitory factor was significantly attenuated in LPA(2)(-/-) mice with reduced infiltration by macrophages. These results show that LPA is capable of promoting tumorigenesis in the colon," wrote S.B. Lin and colleagues, Emory University, Medical Department. The researchers concluded: "The absence of LPA(2) attenuates several effects that contribute to cancer progression in vivo, and, hence, the current study identifies LPA(2) as an important modulator of CC." Lin and colleagues published their study in Gastroenterology (The Absence of LPA(2) Attenuates Tumor Formation in an Experimental Model of Colitis-Associated Cancer. Gastroenterology, 2009;136(5):1711-1720). For additional information, contact C.C. Yun, Emory University, School Medical, Dept. of Medical, Division Digestive Diseases, Whitehead Bldg Suite 201, 615 Michael St., Atlanta, GA 30322, USA. The publisher's contact information for the journal Gastroenterology is: W B Saunders Co-Elsevier Inc., 1600 John F Kennedy Boulevard, Ste. 1800, Philadelphia, PA 19103-2899, USA. Keywords: United States, Atlanta, Adenomatous Polyposis Coli, Colitis, Colon Cancer, Colon Carcinoma, Endocrinology, Experimental Model, Gastroenterology, Genetics, Inflammation, Oncology, Emory University, Medical Department. This article was prepared by Clinical Oncology Week editors from staff and other reports. Copyright 2009, Clinical Oncology Week via NewsRx.com.
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