Abstract
Aberrant glycosylation associated with oncogenic transformation in experimental as well as human cancers was originally indicated by the change of glycolipid profile in virally transformed cells in vitro in 1968, 1969 (Hakomori and Murakami, 1968; Mora et al., 1969), and by the accumulation of fucose- and GlcNAc-containing glycolipids in human cancer in 1964 (Hakomori and Jeanloz); these glycolipids were identified later as Lex, Lea, and Leb, regardless of host Lewis blood group status (Hakomori and Andrews, 1970; Yang and Hakomori, 1971). The first unequivocal evidence that glycolipids were tumor-associated antigens (TAAs) was provided in 1977 by the observed accumulation of asialo-GM2 (Gg3) in KiMSV sarcoma in Balb/c mice and by the fact that rabbit anti-Gg3 antibodies specifically stained KiMSV sarcoma cells grown in vivo, but did not stain a variety of other Balb/c cells and tissues (Rosenfelder et al., 1977), except a few cells in spleen and testis (Hakomori et al., 1980). The concept that TAAs are often carbohydrates evolved only after successful application of the monoclonal antibody (MAb) approach in analysis of TAAs expressed in human cancers. During the past decade, studies with specific MAbs have shown that many TAM are carbohydrates, particularly bound to lipids (glycosphingolipids; GSLs) (see, for reviews, Hakomori and Kannagi, 1983; Hakomori, 1985). The general concept for the immunochemical basis of TAAs is summarized in Table1.
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Hakomori, Si. (1992). Tumor-Associated Carbohydrate Markers. In: Sell, S. (eds) Serological Cancer Markers. Contemporary Biomedicine, vol 11. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-4612-0401-5_10
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DOI: https://doi.org/10.1007/978-1-4612-0401-5_10
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