Relative Expression Of Vitamin D Hydroxylases, CYP27B1 And CYP24A1, And Of Cyclooxygenase-2 And Heterogeneity Of Human Colorectal Cancer In Relation To Age, Gender, Tumor Location, And Malignancy: Results From Factor And Cluster Analysis. - Info and Reading Options

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This article is from <a href="//archive.org/search.php?query=journaltitle%3A%28Cancers%29" rel="nofollow">Cancers</a>, <a href="//archive.org/search.php?query=journaltitle%3A%28Cancers%29%20AND%20volume%3A%284%29" rel="nofollow">volume 4</a>.<h2>Abstract</h2>Previous studies on the significance of vitamin D insufficiency and chronic inflammation in colorectal cancer development clearly indicated that maintenance of cellular homeostasis in the large intestinal epithelium requires balanced interaction of 1,25-(OH)2D3 and prostaglandin cellular signaling networks. The present study addresses the question how colorectal cancer pathogenesis depends on alterations of activities of vitamin D hydroxylases, i.e., CYP27B1-encoded 25-hydroxyvitamin D-1α-hydroxylase and CYP24A1-encoded 25-hydroxyvitamin D-24-hydroxylase, and inflammation-induced cyclooxygenase-2 (COX-2). Data from 105 cancer patients on CYP27B1, VDR, CYP24A1, and COX-2 mRNA expression in relation to tumor grade, anatomical location, gender and age were fit into a multivariate model of exploratory factor analysis. Nearly identical results were obtained by the principal factor and the maximum likelihood method, and these were confirmed by hierarchical cluster analysis: Within the eight mutually dependent variables studied four independent constellations were found that identify different features of colorectal cancer pathogenesis: (i) Escape of COX-2 activity from restraints by the CYP27B1/VDR system can initiate cancer growth anywhere in the colorectum regardless of age and gender; (ii) variations in COX-2 expression are mainly responsible for differences in cancer incidence in relation to tumor location; (iii) advancing age has a strong gender-specific influence on cancer incidence; (iv) progression from well differentiated to undifferentiated cancer is solely associated with a rise in CYP24A1 expression.

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