Expression of human tumor-associated antigens in pancreatic cancer induced in Syrian hamsters
Our previous studies have shown that pancreatic cancer induced in Syrian hamsters by N-nitrosobis(2-oxopropyl)amine (BOP) shows remarkable similarities with the human disease in morphologic and biologic characteristics. Moreover, both human and hamster pancreatic cancer share expression of some tumo...
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Veröffentlicht in: | The American journal of pathology 1990-03, Vol.136 (3), p.707-715 |
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Zusammenfassung: | Our previous studies have shown that pancreatic cancer induced in Syrian hamsters by N-nitrosobis(2-oxopropyl)amine (BOP) shows remarkable similarities with the human disease in morphologic and biologic characteristics. Moreover, both human and hamster pancreatic cancer share expression of some tumor-associated antigens, such as those with blood group specificities, including A, B, H, Leb, Lex, and Ley. By examining other antigens commonly expressed in human pancreatic cancer, we have found that monoclonal antibodies CO17-1A (recognizing 17-1A antigen), OC 125 (recognizing CA 125 antigen), B72.3 (recognizing TAG-72 and DU-PAN-2 react with induced pancreatic cancer in a pattern similar to that seen in human pancreatic cancer. Remarkably, although the epitopes of the antigens recognized by these three antibodies are different, many tumor cells were reactive with all these antibodies. However, in contrast to the human cancer, none of these antigens were expressed in the normal hamster pancreatic tissue, except for 17-1A. However, all of these antigens were expressed in some hamster tissues showing the same cellular localization as pancreatic cancer cells and corresponded, to a great extent, with findings in human tissue. Expression of these antigens was diminished in vitro (cell culture) but was regained in vivo (homologous transplantation). The results emphasize the usefulness of this experimental model for studying some aspects of tissue antigenicity, particularly as it relates to pancreatic cancer. |
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ISSN: | 0002-9440 1525-2191 |