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Cell kinetics and immunogenicity of lymphoma cells treated with 5‐(3,3‐dimethyl‐1‐triazeno) imidazole‐4‐carboxamide (DIC) in vivo
Author(s) -
Silvestrini R.,
Testorelli C.,
Goldin A.,
Nicolin A.
Publication year - 1977
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910190510
Subject(s) - immunogenicity , immune system , in vivo , lymphoma , antigen , cell cycle , in vitro , cancer research , biology , dna synthesis , neoplasm , cell culture , mitosis , cell , immunology , microbiology and biotechnology , biochemistry , genetics
Abstract A cycle of treatment with antineoplastic compounds may alter the immunologic properties of experimental tumors leading to an increased survival of syngeneic hosts as compared to that observed with the original parental tumors. However, a loss of growth potential in drug‐treated tumors might account for this preferential rejection by syngeneic or by allogeneic animals. In the present study the cell cycle kinetics of parental (L1210 and L5178Y) and DIC‐altered leukemic cells (L1210/DIC; L5178Y/DIC) has been evaluated by the establishment of labelled mitosis curves. The in vitro DNA synthesis and cell loss were also investigated. The experimental results indicate that no significant differences in the above properties were present for parental and corresponding drug‐treated leukemic sublines. Immunodepressed allogeneic mice were more resistant to lymphoma challenge when inoculated with the DIC‐sublines than with the parental lines. On adoptive transfer of immune lymphocytes there was increased survival of allogeneic animals challenged with DIC cells, attributable to an additional immune response to DIC‐induced antigens. Thus, parental or DIC‐tumors showed similar tumorigenic characteristics, and the increased allogeneic host survival to DIC‐cell challenge may be attributed to an additional immune response of the animal against DIC‐induced antigens.