Since 1960, the L2C leukemia has been employed for a variety of virologic, chemotherapeutic, and immunotherapeutic studies. Until now, it was assumed that L2C leukemias of the different laboratories were identical cell lines. However, contrasting data have been published concerning the immunogenicity of L2C cells in syngeneic hosts and their proliferation in allogeneic animals. Cytogenetic variations between BZ-L C and LE-L2C have also been reported. In the present paper, the karyotypes of 4 of the 5 L2C lines were examined in detail to determine whether or not the various lines are derived from an identical ancestral line, and if noticeable chromosomal differences could explain the immunologic variations. The comparison of the different L2C chromosome banding patterns with the banding patterns of normal guinea pig chromosomes made it possible to determine the origin of the various chromosomal markers of the leukemic cell line studied. It appeared that the 4 cell lines (GH-L2C, EN-L2C, BZ-L*C and LG-L2C) generally had near diploid chromosome numbers ranging from 60 to 66 with the majority of the cells having 65 chromosomes. Line EN-L2C had chromosome numbers ranging from 63 to 66 with approximately equal numbers of cells having 64, 65, and 66 chromosomes. Chromosome numbers of BZ-L*C ranged from 61 to 65 with most cells having 64 chromosomes. The majority of the cells of the LG-L2C line had 64 chromosomes, with a range from 63 to 65 chromosomes. Only the line GH-L2C has the 2q-marker and is positive for C3 receptors, which seems peculiar. Since resolution of the G-bands is poor, there could be differences in the deleted portion not detectable by the present technique. It may also be simply that the C3 receptor is determined by complex genic interaction that cannot be explained by a missing site on a single chromosome, in this case 2q-. Otherwise, there is no apparent correlation between immuno-characteristics and the presence or absence of chromosomal markers. This failure to demonstrate a relation may represent gene mutation, gene recombination, or structural rearrangement as an explanation for resulting immunologic differences between these leukemic cell lines.
|Number of pages||5|
|Publication status||Published - Dec 1 1977|
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