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Identification by Monoclonal Antibody of the Tumor Antigen of a Human Autologous Breast Cancer Cell That Is Involved in Cytotoxicity by a Cytotoxic T-Cell Clone¹

Department of Pathology [M. O., N. S., Y. W., S. T., K. T., N. T., K. K.] and Department of Surgery [T. S., M. O., K. A.], Sapporo Medical College, 060 Sapporo, Japan

We have already established a pair of human autologous clones, tumorspecific cytotoxic T-lymphocyte clone T_cHMC-1 and tumor target clone HMC-1-8, that were derived from the metastatic pleural effusion of a patient with mammary carcinoma. In this paper, we describe the target antigen that was defined by monoclonal antibody 3A2. This monoclonal antibody selectively inhibited the cytotoxic action of T_cHMC-1 against HMC1-8 autologous tumor target cells, but not the cytotoxicity of lymphokine-activated killer and possibly natural killer cells against HMC-1-8 cells. Western blot analysis using the 3A2 monoclonal antibody identified a molecule with an approximate molecular weight of 92,000. This antigen was highly expressed on autologous primary cancer cells of breast carcinoma tissue, but not on the normal mammary gland in the same patient. Moreover, this antigen can be detected on approximately 50% of human allogeneic breast carcinomas, but not on other neoplastic tissues such as gastric and colonic carcinomas except for one out of 10 prostatic carcinomas. Nonneoplastic normal cells did not express this antigen. It was also suggested that the antigen is not murine mammary tumor virus-related products. These data suggest that 3A2-defined antigen could participate in the cytotoxicity by human autologous cytotoxic T-lymphocytes as the target molecule expressed on tumor cells.

¹ This work was supported by a Research Grant of the Princess Takamatsu Cancer Research Fund and a Grant-in-Aid for Special Project Research by Biotechnology.

² To whom requests for reprints should be addressed, at Department of Pathology, Sapporo Medical College, S. 1, W. 17, Chuo-ku, 060 Sapporo, Japan.

Received 1/17/89. Revised 4/10/89. Accepted 4/19/89.

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