NewsRx.com
October 8, 2009
According to recent research from Vienna, Austria, "Sporadic colorectal cancer is a disease of advancing age and the percentage of the population which reaches an advanced age is strongly, increasing. Multiple factors are responsible for the etiology of this cancer since the colorectal mucosa is directly influenced by, nutrients reaching the colonic lumen and impacting on mucosal cells."
"The vitamin D system appears to be central to several preventative molecular pathway's. Insufficiency of the serum precursor 25-hydroxyvitamin D-3 has been linked by, epidemiology to enhanced colon tumor incidence, most likely because it is a major determinant (if 1,25-dihydroxyvitamin D-3 synthesis in colonic mucosal cells. Bound to its receptor, vitamin D regulates colonic pro lift ration, differentiation and apoptosis in an autocrinel/paracrine manner. During early malignancy, vitainin D synthesis is enhanced to counteract hyperproliferation, whereas in high-grade tumors catabolism by far surpasses synthesis. The colonic vitamin D system is regulated by, several known natural factors. One of the most important ones is nutritional calcium that, if supply, is low, will result in enhanced catabolism of colonic 1,25dihydroxyvitamin D3. Estrogenic compounds can increase expression and activity, of the synthesizing 25-hydroxyvitamin D-1 alpha-hydroxylase. Due to enhanced synthesis of the active metabolite, this can lead to protection against colorectal tumors in women. During tumor progression, expression of 25-hydroxyvitamin D-1 alpha-hydroxylase as well as of the catabolizing 25-hydroxyvitamin D-24-hydroxylase appears to be under epigenetic control as demonstrated by studies with phytoestrogens and folate. It is commonly accepted that sporadic colorectal cancer pathogenesis is multifactorial and these are just a few examples of the regulatory, capacity of natural (nutrient) substances for improving the colonic vitamin D system. However, protection by vitantin D might have central importance, with nutrients increasing the efficiency, of the vitamin D system in a targeted manner," wrote H.S. Cross and colleagues, Medical University of Vienna.
The researchers concluded: "This could result in prevention of hyperproliferation or retardalion of progression to clinically, manifest primary colonic tumors."
Cross and colleagues published their study in Anticancer Research (Modulation of Vitamin D Synthesis and Catabolism in Colorectal Mucosa: A New Target for Cancer Prevention. Anticancer Research, 2009;29(9):3705-3712).
For additional information, contact H.S. Cross, Medical University of Vienna, Dept. of Pathophysiology, Waehringer Guertel 18-20, A-1090 Vienna, Austria.
Publisher contact information for the journal Anticancer Research is: International Institute Anticancer Research, Editorial Office 1ST km Kapandritiou-Kalamou Rd. Kapandriti, PO Box 22, Athens 19014, Greece.
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