TY - JOUR
T1 - Triplication of one chromosome no. 15 with an altered C‐myc containing ecori fragment and elimination of the normal homologue in a T‐cell lymphoma line of akr origin (TIKAUT)
AU - Wirschubsky, Zvi
AU - Wiener, Francis
AU - Spira, Jack
AU - Sümegi, Janos
AU - Klein, George
PY - 1984/4/15
Y1 - 1984/4/15
N2 - An ouabain‐ and thioguanine‐resistant subline (TIKAUT) of spontaneous AKR lymphoma, TKA, was trisomic for chromosome 15 and contained a single 33 kb EcoRI fragment, containing the oncogene c‐myc. The original TKA lymphoma and derived in vitro line contained the same 33 kb fragment, as well as a normal 22 kb fragment. It has been concluded that the original 15‐trisomic TKA tumor has duplicated a 15‐chromosome that contained the changed fragment, while maintaining the normal fragment as well. Subsequently, in the derived TIKAUT line, the changed chromosome duplicated again, giving rise to three copies, and the normal homologue was eliminated altogether. This confirms our earlier somatic hybrid study showing that the duplicated 15‐chromosome of a T‐cell leukemia confers an advantage on the cell that favors tumorigenicity, whereas the normal homologue exerts a counteracting influence. Therefore, in the course of tumor progression, the changed chromosome tends to be amplified, whereas its normal homologue tends to be eliminated.
AB - An ouabain‐ and thioguanine‐resistant subline (TIKAUT) of spontaneous AKR lymphoma, TKA, was trisomic for chromosome 15 and contained a single 33 kb EcoRI fragment, containing the oncogene c‐myc. The original TKA lymphoma and derived in vitro line contained the same 33 kb fragment, as well as a normal 22 kb fragment. It has been concluded that the original 15‐trisomic TKA tumor has duplicated a 15‐chromosome that contained the changed fragment, while maintaining the normal fragment as well. Subsequently, in the derived TIKAUT line, the changed chromosome duplicated again, giving rise to three copies, and the normal homologue was eliminated altogether. This confirms our earlier somatic hybrid study showing that the duplicated 15‐chromosome of a T‐cell leukemia confers an advantage on the cell that favors tumorigenicity, whereas the normal homologue exerts a counteracting influence. Therefore, in the course of tumor progression, the changed chromosome tends to be amplified, whereas its normal homologue tends to be eliminated.
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U2 - 10.1002/ijc.2910330410
DO - 10.1002/ijc.2910330410
M3 - Article
C2 - 6323325
AN - SCOPUS:0021345778
SN - 0020-7136
VL - 33
SP - 477
EP - 481
JO - International Journal of Cancer
JF - International Journal of Cancer
IS - 4
ER -