These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Are methylcholanthrene-induced sarcoma-associated, rejection-inducing (TSTA) antigens, modified forms of H-2 or linked determinants?
    Author: Klein G, Klein E.
    Journal: Int J Cancer; 1975 Jun 15; 15(6):879-87. PubMed ID: 50291.
    Abstract:
    TA3Ha/MSWBS hybrid cells have been derived from the fusion of the TA3Ha ascites carcinoma (H-2a) and the methylcholanthrene-induced MSWBS ascites sarcoma (H-2s). MSWBS expresses a strong tumor-specific transplantation antigen (TSTA), capable of inducing a rejection reaction in the syngeneic A.SW host. The genetic determinants of the H-2 complex are known to be localized on chromosome No. 17. TA3Ha contributes two normal, telocentric chromosomes No. 17 to the hybrid. In contrast, both chromosomes No. 17 of MSWBS are localized on readily identifiable translocations (17/1 and 17/M1 ; see Wiener et al., 1974). We have previously shown that the chromosomes No. 17 of one parental strain, or the other (but not both) can be removed from the hybrid by selective passage in the opposite parental strain. The present paper examined the possibility, often suggested in the literature, that the MC-sarcoma-associated TSTA could be a modified form of H-2. MSWBS, unselected TA3Ha/MSWBS and YACIR/MSWBS hybrids were compared with TA3Ha/MSWBS-derived isoantigen loss variants, with regard to their immunogenicity in the TSTA test, i.e. their ability to induce rejection of MSWBS target cells in ASW mice. Whereas the unselected hybrids were as immunogenic as the parental MSWBS line itself, two strain A compatible and two strain A.SW compatible variants which had lost chromosome No. 17 of the opposite strain showed a residual, but clearly weakened immunogenicity. Since there was no systematic difference between the reciprocal types, it is concluded that the genetic determinant of TSTA is not localized on the chromosome No. 17 but that a proper balance of this chromosome is required for the full expression of immunogenicity in the TSTA system.
    [Abstract] [Full Text] [Related] [New Search]