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1998 Abstract: IMMUNOHISTOCHEMICAL ASSESSMENT OF 17-1A AND COMPLEMENT RESISTANCE FACTORS CD55 AND CD59 IN ESOPHAGEAL CANCER. S.B. Hosch, S. Inndorf, S. Bull, F. Stern, K. Pantel, J.R. Izbicki. Departments of Surgery, University of Hamburg, and Immunology, University of Munich, Germany. 62

Abstracts
1998 Digestive Disease Week

#966

IMMUNOHISTOCHEMICAL ASSESSMENT OF 17-1A AND COMPLEMENT RESISTANCE FACTORS CD55 AND CD59 IN ESOPHAGEAL CANCER. S.B. Hosch, S. Inndorf, S. Bull, F. Stern, K. Pantel, J.R. Izbicki. Departments of Surgery, University of Hamburg, and Immunology, University of Munich, Germany.

Background: Dissemination of immunohistochemically identifiable isolated tumor cells to lymph nodes of patients with esophageal cancer is an independent predictor for tumor relapse after curative surgical treatment. In consideration of the minimal residual tumor load these patients might benefit from an adjuvant therapy with the monoclonal antibody 17-1A, which has shown to be effective in preventing tumor relapse in patients with colon cancer. However, there is evidence that the presence of complement resistance factors inhibit complement dependent cytotoxicity in patients treated with monoclonal antibodies.

Methods: We therefore examined the expression of 17-1A antigen and the membrane bound complement resistance factors CD55 and CD59 on primary tumors of 62 consecutive patients with esophageal cancer who had undergone radical en-bloc esophagectomy using immunohistochemical assays with monoclonal antibodies directed against 17-1A, CD55, and CD59.

Results: 29 patients (47%) showed a homogeneous expression of 17-1A, whereas 19 patients (31%) had a heterogeneous staining pattern and 14 patients (22%) showed no expression of 17-1A antigen. 14 patients (48%) with homogeneous 17-1A expression were negative for CD55 expression whereas 11 patients (38%) with homogeneous 17-1A expression displayed CD55 heterogeneously and 4 patients (14%) displayed CD55 homogeneously.
13 patients (68%) who expressed the 17-1A antigen heterogeneously had no CD55 expression, 6 patients (32%) showed heterogeneous CD55 expression, and none of these patients displayed homogeneous CD55 expression. Furthermore expression of CD59 was absent in 14 patients (48%) with homogeneous 17-1A expression compared to 9 patients (31%) with a heterogeneous and 6 patients (21%) with a homogeneous expression of CD59. Similar results for CD59 expression were observed in the group of patients with heterogeneous 17-1A expression.

Conclusions: Our data indicate that about 80% of esophageal cancer patients display 17-1A antigen on their primary tumors and therefore might be suitable candidates for an adjuvant 17-1A antibody therapy. However, a substantial fraction of these patients display complement resistance factors, which might inhibit the efficacy of the antibody treatment. Consequently immuno-histochemical assessment of these factors on primary tumors and micrometastases could be helpful to identify those patients, who might benefit from such therapeutic strategies.

Copyright 1996 - 1998, SSAT, Inc. Revised 29 June 1998.



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