Abstract
A major limitation to the clinical efficacy of cisplatin is the intrinsic or acquired resistance of many neoplasms to the drug. As a result, many studies to investigate the mechanisms of cisplatin resistance have been carried out with human and rodent cells in culture. Acquired resistance has been ascribed in different cases to changes in drug accumulation, intracellular drug inactivation by enhanced levels of glutathione or metallothionein, and enhanced DNA repair.
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Wood, R.D., Vilpo, J.A., Vilpo, L.M., Szymkowski, D.E., O’Donovan, A., Moggs, J.G. (1996). Hypersensitivity to Cisplatin in Mouse Leukemia L1210/0 Cells: An XPG DNA Repair Defect. In: Pinedo, H.M., Schornagel, J.H. (eds) Platinum and Other Metal Coordination Compounds in Cancer Chemotherapy 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0218-4_30
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DOI: https://doi.org/10.1007/978-1-4899-0218-4_30
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