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Cessation of autonomous proliferation of mouse lymphoma EL4 by fusion with a T cell line
Author(s) -
Kubota Koichi,
Katoh Hideki
Publication year - 1990
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.2910450328
Subject(s) - lymphoma , cell culture , cancer research , cell growth , fusion , biology , immunology , medicine , pathology , virology , genetics , philosophy , linguistics
Benzanthracene‐induced C57BL/6 (H‐2 b ) mouse T‐cell lymphoma EL4 (a thymidine kinase‐deficient cell line) was fused by using polyethylene glycol with an Mls a (Mls for minor lymphocyte stimulatory) antigen‐dependent T cell line, which was designated G4 and had been derived from a C3H/He mouse (H‐2 k ), and the fused cells were cultured in HAT medium. Although no growing cells appeared in most of these fusions, we consistently obtained growth‐arrested H‐2K b ‐positive cells from the fused cell populations by the panning method. The cells were tetraploid and were able to proliferate in response to Mls a antigen. Three H‐2K b ‐positive clones, isolated by limiting dilution from three different fusions, were shown to be EL4 × G4 hybrids, because (I) they had both H‐2 k and H‐2 b antigens; (2) each of the clones had one submetacentric chromosome which was a marker chromosome of EL4, and they were tetraploid with modal chromosome numbers of 74, 78, and 79, respectively; (3) they had 4 isozymes of both parental cells. These results indicate that EL4 lymphoma cells cease to proliferate when fused with T cell line G4. The malignant phenotype of lymphoma EL4 is thus suppressed at the level of cell transformation by the introduction of the G4 cell genome.