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Coexpression of MUC1 Glycoprotein with Multiple Angiogenic Factors in Non-Small Cell Lung Cancer Suggests Coactivation of Angiogenic and Migration Pathways¹

Department of Pathology, Democritus University of Thrace, Alexandroupolis 68100, Greece [A. G., E. S.]; Department of Radiotherapy/Oncology, University of Thessalia, Medical School, Larisa, Greece[M. I. K.]; Department of Oncology, Leicester Royal Infirmary, Leicester LE1 5WW, United Kingdom [K. O., G. C.]; Department of Pharmacology, University of Texas Southern Medical Center, Dallas, Texas 75235-9041[P. E. T.]; and Departments of Cellular Science and Imperial Cancer Research Fund-Medical Oncology Unit, Oxford Radcliffe Hospital, Headington, Oxford OX3 7LJ, United Kingdom [K. C. G., A. L. H.]

We investigated the expression of MUC1 protein and its relationship to the microvessel density and the expression of thymidine phosphorylase, vascular endothelial growth factor (VEGF), VEGF-receptor KDR, basic fibroblast growth factor (bFGF), and bFGF-receptor (FGFR-2) in non-small cell lung cancer. Although MUC1 expression was found equally in poorly and highly vascularized tumors, a significant coexpression with multiple angiogenic factors and their receptors was noted (P = 0.0002, 0.03, 0.19, 0.10, and 0.01 for thymidine phosphorylase, VEGF, KDR, bFGF, and FGFR-2, respectively). In multiple regression analysis, both angiogenesis and MUC1 expression were independent prognostic variables. The present study suggests the existence of an early genetic event leading to the activation of both migration and angiogenesis pathways in non-small cell lung cancer.

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