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Finally, mice immunized with syngeneic tumors demonstrated an apparent prolongation of certain skin allografts. The discussion considers possible alternatives explaining these results. Chemically induced tumors usually possess detectable tumor-specific transplantation antigens TSTA , which are generally considered to be specific for the individual tumors 27, 36, The genesis of these tumor antigens and their biological function s has been the subject of many investigations 29, 30, It has been proposed that TSTA have resulted from the re-expression or amplification of normal embryonic cellular components The original observation that the carcinoem-bryonic antigen was specific for colon adenocarcinomas tended to support this hypothesis Subsequently, it was found that carcinoembryonic antigen was associated with a variety of gastrointestinal neoplasms and inflammatory diseases of the gut 18 , thus casting serious doubt on the tumor-specific nature of carcinoembryonic antigen.

Further evidence which de-emphasizes the relationship between embryonic antigens and TSTA has been presented by Baldwin et al. An alternative hypothesis was that TSTA were related to histocompatibility antigens that were normally expressed in allogeneic strains 7, 25, 33, Evidence supporting a relationship between TSTA and histocompatibility antigens has been suggested by experiments which showed that both TSTA and histocompatibility antigens can induce transplantation immunity 9, 22 , demonstrate a high degree of polymorphism 4, 17 , and have a reciprocal relationship of the cell surface 19, If this hypothesis is valid, there will exist certain FI hybrids in which a parental strain tumor will be poorly immunogenic because of the cross-reactivity of the TSTA and the histocompatibility antigens of the F1, and therefore in which the tumor will grow better than it does in the syngeneic parent.

This phenomenon has been demonstrated by Huemer 23, 24 , Invernizzi and Parmiani 25 , Parmiani and Invernizzi 33 , and Rumma and Davies Their findings were in contrast to the more common observation that parental strain tumors generally elicit a stronger immune response and grow more poorly in the F, hybrid 44— Futher support for the hypothesis was gained by the demonstration that certain normal allogeneic tissues protected selected parental strains against syngeneic tumor growth The reciprocal experiments, that is immunizing with the sarcomas and challenging with allogeneic skin, resulted in accelerated graft rejection by the appropriate strains These investigations taken collectively seemed to support the hypothesis that TSTA, in certain instances, cross-reacted with allogeneic histocompatibility antigens.

The possible mechanisms for the expression of alloantigens on tumor cells have been postulated to result from mutations at the level of the histocompatibility genes by the carcinogen 32, 34 , or that the normal genome may contain structural genes coding for these antigens, but that these genes are repressed in the normal cell and become expressed only during neoplastic transformation.

Garrido et al. The Ly system of antigens may be another example of such a situation This latter hypothesis implies that the genome of each animal of the species may contain the structural information for many or all of the histocompatibility antigens of that species, and if correct would have profound effects on the concepts concerning the biological functions of these antigens 6. You may be trying to access this site from a secured browser on the server. Please enable scripts and reload this page. Wolters Kluwer Health may email you for journal alerts and information, but is committed to maintaining your privacy and will not share your personal information without your express consent.

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