A novel tumor-associated antigen expressed in human uterine and ovarian carcinomas

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Abstract
BACKGROUND A large number of monoclonal antibodies (MoAbs) against human tumor cells have been generated and it has been shown that these MoAbs are useful tools in the diagnosis and treatment of cancer patients, as well as in the basic investigation of the oncogenesis and characterization of cancer cells. METHODS The 22‐1‐1 MoAb was established by cell fusion between mouse myeloma cells and spleen cells derived from mice immunized with the human uterine cervical adenocarcinoma cell line, SiSo. The tissue distribution and biologic characteristics of the 22‐1‐1 antigen (Ag) were examined. RESULTS The 22‐1‐1 Ag was distinct from the known tumor‐associated antigens such as YH 206, GA 733, CA 125, carcinoembryonic antigen, and sialyl Lex molecules in an expression pattern in human tumor cell lines. An immunohistochemical study revealed that 22‐1‐1 Ag was expressed in 87.5% of uterine cervical adenocarcinomas, 66% of uterine endometrial adenocarcinomas, and 58.8% of ovarian carcinomas. Moreover, 22‐1‐1 Ag was detected in 87.7% of uterine cervical squamous cell carcinomas; however, it was not detected in normal uterine cervical or ovarian tissues, except in uterine endometrial glands, in which its expression was observed at low levels. The 22‐1‐1 Ag was secreted into cell culture supernatant fluids and was also detected in the vaginal discharges of uterine cervical carcinoma patients. The antigenic epitope of 22‐1‐1 Ag was shown to be a protein with a molecular weight of 78 kilodaltons using sodium dodecyl sulfate‐polyacrylamide gel electrophoresis analysis. CONCLUSIONS The 22‐1‐1 MoAb reactive to a novel tumor‐associated antigen was generated. This Ag was expressed in cancer cells derived mainly from the uterus and ovary. Moreover, 22‐1‐1 Ag was secreted in the vaginal discharges of uterine cervical carcinoma patients. 22‐1‐1 MoAb is a potential tool for the study of oncogenesis and the management of cancer patients. Cancer 1996; 77:1501‐9.