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Characterization of a Malignant Phenotype-associated Cell Surface Glycoprotein Common to Various Human Tumor Cells and Preferentially Expressed on Adenocarcinoma of the Lung¹

Molecular Hepatology Laboratory, The Cancer Center, Massachusetts General Hospital, Charlestown, Massachusetts 02129, and the Department of Medicine, Harvard Medical School, and the Harvard-MIT Division of Health Science, Boston, Massachusetts 02114

Since both the liver and lung are derived from the endoderm, common antigens may appear on both tissues during malignant transformation. In an attempt to delineate cell surface alterations associated with the neoplastic transformation of these tissues, we have produced a library of monoclonal antibodies against a human hepatoma cell line termed FOCUS. One of these monoclonal antibodies, designated AF-10, recognized an antigen preferentially expressed on human lung adenocarcinoma cells, both in vitro and in vivo. This antigen has been characterized using Western immunoblot analysis and immunoprecipitation from surface-iodinated or metabolically labeled cells. The mature antigen is a cell surface glycoprotein with a core polypeptide with a molecular weight of 75,000 bearing N-glycosylation units. This protein migrates in sodium dodecyl sulfate-polyacrylamide gel electrophoresis with an apparent molecular weight of 100,000–115,000 in reducing conditions and M_r 115,000–130,000 in nonreducing conditions. The epitope recognized by monoclonal antibody AF-10 is borne by the core protein. This antigen is shed from the cell surface and was identified in the culture supernatant from lung adenocarcinoma cell lines. Studies of the biodistribution of the AF-10 antigen showed that it was also expressed at low levels in normal human small intestine and kidney. The AF-10 monoclonal antibody may be useful for the study of the antigen expression between normal lung and the transformed phenotype.

¹ This work was supported by Grants CA-35711, AA-02666, and HD-20469 from the National Institute of Health.

² Recipient of a Research Fellowship from the Association pour la Recherche sur le Cancer, Villejuif, the Société Française de Cancérologie, Paris, France, and from the Arthur Sachs Foundation, Harvard University, Cambridge, Massachusetts.

³ Recipient of a Research Scientist Developmental Award AA-00048. To whom requests for reprints should be addressed, at Molecular Hepatology Laboratory, The Cancer Center, Massachusetts General Hospital East, 7th Floor, 149 13th Street, Charlestown, MA 02129.

Received 7/ 6/88. Accepted 12/ 9/88.