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Loss of Annexin 1 Correlates with Early Onset of Tumorigenesis in Esophageal and Prostate Carcinoma

Division of Therapeutic Products, Center for Biologics Evaluation Research, Food and Drug Administration, Bethesda, Maryland 20892 [C. P. P., V. E. B., V. S. C., E. F. P.]; Georgetown University, Department of Chemistry, Washington, DC 20057 [C. P. P.]; Laboratory of Pathology [C. P. P., V. E. B., S. M. H., P. H. D., L. A. L.], Urologic Oncology Branch [D. K. O., C. D. V., W. M. L.], Pathogenetics Unit, Laboratory of Pathology [D. K. O., M. R. E-B.], Cancer Prevention Studies Branch [M. J. R., N. H., P. R. T.], and Cancer Genome Anatomy Project, Office of the Director [J. W. G.], National Cancer Institute, NIH, Bethesda, Maryland 20892; National Naval Medical Center, Bethesda, Maryland 20892 [J. H.]; and Pathology Laboratory, Shanxi Cancer Hospital, Taiyuan 030013, China [Q-H. W.]

Annexin I protein expression was evaluated in patient-matched longitudinal study sets of laser capture microdissected normal, premalignant, and invasive epithelium from human esophageal squamous cell cancer and prostatic adenocarcinoma. In 25 esophageal cases (20 by Western blot and 5 by immunohistochemistry) and 17 prostate cases (3 by Western blot and 14 by immunohistochemistry), both tumor types showed either complete loss or a dramatic reduction in the level of annexin I protein expression compared with patient-matched normal epithelium (P 0.05). Moreover, by using Western blot analysis of laser capture microdissected, patient-matched longitudinal study sets of both tumor types, the loss of protein expression occurred in premalignant lesions. Concordance of this result with immunohistochemical analysis suggests that annexin I may be an essential component for maintenance of the normal epithelial phenotype. Additional studies investigating the mechanism(s) and functional consequences of annexin I protein loss in tumor cells are warranted.

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