DNA repair in cisplatin-sensitive and resistant human cell lines measured in specific genes by quantitative polymerase chain reaction.
More than 80% of patients with testicular germ cell tumours (TGCT) are cured using cisplatin-based combination chemotherapy, and resistance to cisplatin is the final barrier to the cure of nearly all patients with this disease. In this study, we used quantitative polymerase chain reaction (Q-PCR) to investigate the role of DNA repair in cisplatin resistance in two genes, one transcribed and one not transcribed. Three pairs of cisplatin-sensitive and resistant cell lines were used, two derived from TGCT and one from a bladder cancer. In these pairs of sublines, we observed no major differences between the repair of cisplatin-induced damage in the transcribed and nontranscribed genes, nor did there appear to be any relationship between DNA repair capacity and the development of cisplatin resistance. Despite the strong indication that the sensitivity of testis tumour cells to cisplatin is related to their reduced ability to repair cisplatin-damaged DNA, these cells apparently do not become resistant to cisplatin by acquiring DNA repair capacity.
Köberle
B
B
University College London, Institute of Urology and Nephrology, U.K.
Payne
J
J
Grimaldi
K A
KA
Hartley
J A
JA
Masters
J R
JR
D000970:Antineoplastic Agents / Q000494:pharmacology*; D002945:Cisplatin / Q000493:pharmacokinetics / Q000494:pharmacology*; D004260:DNA Repair; D004351:Drug Resistance; D006801:Humans; D016133:Polymerase Chain Reaction; D014407:Tumor Cells, Cultured
D000970:Antineoplastic Agents; D002945:Cisplatin