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[Cancer Research 54, 3120-3123, June 15, 1994]
© 1994 American Association for Cancer Research

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Inverse Relation of E-Cadherin and Autocrine Motility Factor Receptor Expression as a Prognostic Factor in Patients with Bladder Carcinomas1

Thomas Otto, Walter Birchmeier2, Ulrich Schmidt, Axel Hinke, Jörg Schipper, Herbert Rübben and Avraham Raz3

Department of Urology [T. O., A. H., H. R.], Institute of Cell Biology (Tumor Research) [W. B.], Institute of Pathology [U. S.], Department of Otorhinolaryngology [J. S.], University of Essen, Medical School, Hufelandstr. 55, 4300 Essen, Federal Republic of Germany, and Metastasis Research Program, Michigan Cancer Foundation, Departments of Pathology and Radiation Oncology, Wayne State University, Detroit, Michigan 48201 [A. R.]

Down-regulation of E-cadherin, an intercellular adhesion molecule, and up-regulation of autocrine motility factor receptor (gp78) expressions have been shown to play a role in tumor cell invasion and metastasis. Monoclonal antibodies against E-cadherin and gp78 were used to stain serial snap-frozen sections of 12 normal bladder and 83 bladder carcinoma specimens (27 noninvasive, 53 invasive, and 3 metastases). In normal urothelium, E-cadherin is expressed while gp78 is not. Positive expression of E-cadherin and negative expression of gp78 were found to be associated with a low risk of clinical progression in the superficial bladder carcinoma patient group. While reduction in E-cadherin concomitantly with an increase in gp78 expression was associated with poor prognosis, 71% of the patients (n = 30) underwent rapid cancer progression, and 32% of the patients died of cancer-related disease at a median of 2 years after initial diagnosis. Thus, it is suggested that reduction of E-cadherin expression associated with an increase in the level of gp78 in bladder cancers may define a high risk group of patients. The dual use of these two antigens may improve early diagnosis of high risk bladder cancer patients and influence treatment decisions.

1 This work was supported by Deutsche Forschungsgemeinschaft SFB 354 (to T. O., W. B., and H. R.), the Wilhelm Sander-Stiftung (to W. B.), and in part by USPHS Grant 51714 from the National Cancer Institute and the Paul Zuckerman Support Foundation for Cancer Research (to A. R.).

2 Present address: Max Delbruck Cancer Center, Robert-Rossler St., 10, 12132 Berlin, Federal Republic of Germany.

3 To whom requests for reprints should be addressed, at Metastasis Research Program, Michigan Cancer Foundation, 110 East Warren Avenue, Detroit, MI 48201.

Received 3/23/94. Accepted 5/ 4/94.




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Copyright © 1994 by the American Association for Cancer Research.