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Compensatory Occurrence of IV²Fuc,II³NeuAc-Gg₄Cer and Human Fetal Antigen Lc₄Cer in Small Cell Carcinomas of the Human Lung¹

Department of Biochemistry, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo [M. I.]; Department of Obstetrics and Gynecology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo [K. K., S. N.]; Pathology Division, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo [S. H., Y. S.]; and Tokyo Metropolitan Institute of Medical Science, 3-18-22 Honkomagome, Bunkyo-ku, Tokyo [Y. N.], Japan

By means of a thin-layer chromatography immunostaining procedure involving a human monoclonal anti-Lc₄Cer antibody, which was established by hybridizing murine myeloma cells and human lymphocytes from a cancer patient, Lc₄Cer was proven to be a fetal antigen of human lung and to be a cancer-related antigen in small cell carcinomas of human lung, but not of other lung cancers, i.e., large cell carcinomas, adenocarcinomas, and squamous carcinomas. With the simultaneous detection of IV²Fuc,II³NeuAc-Gg₄Cer with rabbit anti-IV²Fuc,II³NeuAc-Gg₄Cer antiserum, the expression of Lc₄Cer and IV²Fuc,II³NeuAc-Gg₄Cer was found to be compensatory and, consequently, small cell lung carcinomas could be classified into Lc₄Cer- and IV²Fuc,II³NeuAc-Gg₄Cer-expressing types, L-SCLC and F-SCLC, respectively, which were detected in four and 27 of 31 patients' tissues and in one and three of four nude mouse-transplanted small cell lung carcinoma tissues, respectively. The compensatory expression of Lc₄Cer and IV²Fuc,II³NeuAc-Gg₄Cer in small cell carcinomas indicated that different metabolic pathways for glycosphingolipids were activated to give the distinct glycosphingolipid compositions in the two types of small cell lung carcinomas.

¹ This work was supported by a Grant-in-Aid for Scientific Research on Priority Areas, No. 04250106, from the Ministry of Education, Science, and Culture, Japan.

² To whom requests for reprints should be addressed.

Received 4/ 2/93. Accepted 10/ 8/93.