Testis tumors are cured using cisplatin-based chemotherapy in over 80%
of patients, and sensitivity to cisplatin is retained by testis tumor
cells in vitro. The aim of this study was to use complementation anal
ysis to determine how many genes control sensitivity to cisplatin in t
estis tumor cells. Four testis tumor cell lines were transfected with
pSV2NEO and pBABE plasmids, conferring G418 and puromycin resistance,
respectively. Self-crosses were generated to control for gene dosage,
and the parentage of the hybrids was confirmed by PCR amplification of
VNTR regions. Karyotyping confirmed that all the hybrids retained at
least 88% of the combined number of chromosomes of the two parental ce
ll lines. Cisplatin sensitivity was measured by clonogenic assay and c
omplementation was not observed. This finding provides evidence that t
here is a single common mechanism controlling cisplatin sensitivity in
testis tumor cells. (C) Elsevier Science Inc., 1997.