TY - JOUR
T1 - Changes of the immunogenic properties of K36 lymphoma treated in vivo with 5(3,3-dimethyl-1-triazeno) imidazole-4-carboxamide (DTIC)
AU - Bonmassar, A.
AU - Frati, L.
AU - Fioretti, M. C.
AU - Romani, L.
AU - Giampietri, A.
AU - Goldin, A.
PY - 1979
Y1 - 1979
N2 - 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.
AB - 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.
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U2 - 10.1016/0014-2964(79)90276-7
DO - 10.1016/0014-2964(79)90276-7
M3 - Article
C2 - 488153
AN - SCOPUS:0018746529
VL - 15
SP - 933
EP - 939
JO - European Journal of Cancer
JF - European Journal of Cancer
SN - 0014-2964
IS - 7
ER -