Changes of the immunogenic properties of K36 lymphoma treated in vivo with 5(3,3-dimethyl-1-triazeno) imidazole-4-carboxamide (DTIC)

A. Bonmassar, L. Frati, M. C. Fioretti, L. Romani, A. Giampietri, A. Goldin

Research output: Contribution to journalArticlepeer-review

Abstract

Mice of AKR strain bearing syngeneic K36 lymphoma were treated with DTIC for a number of transplant generations. The lymphoma line (K36/DTIC) became resistant to DTIC treatment and weakly immunogenic for AKR or (AKR × DBA/2)F1 hosts. Previous findings, however, showed that DTIC-treated H-2b or H-2b lymphomas became DTIC-resistant as well, but acquired strong immunogenicity for histocompatible hosts. Transplantation resistance of allogeneic mice against K36 or K36/DTIC lines injected i.p. or i.v. was also investigated. Both lines inoculated i.p. were rejected by either H-2-incompatible recipients, or H-2-compatible mice incompatible for minor histocompatibility loci (MIH). When the tumors were injected intravenously, H-2-compatible MIH-incompatible mice were more susceptible than H-2-MIH-incompatible recipients to lymphoma challenge. Moreover K36/DTIC line elicited stronger transplantation resistance than K36 tumor. Unexpectedly H-2-MIH-incompatible mice homozygous for the H-2d haplotype were partially susceptible to the i.v. challenge with K36 lymphoma cells. However, strong transplantation resistance was found in the same hosts against K36/DTIC line. In conclusion the limited increase of tumor cell immunogenicity obtained by treatment of K36 lymphoma with DTIC was detectable in syngeneic, hybrid and allogeneic mice.

Original languageEnglish
Pages (from-to)933-939
Number of pages7
JournalEuropean Journal of Cancer (1965)
Volume15
Issue number7
DOIs
Publication statusPublished - 1979

ASJC Scopus subject areas

  • Oncology

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