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Mechanisms of acquired resistance to cisplatin

  • Chapter
Anticancer Drug Resistance

Part of the book series: Cancer Treatment and Research ((CTAR,volume 73))

Abstract

Since the discovery of the antitumor activity in rodents of cisplatin (cis-diamminedichloroplatinum(II)) in 1968 [1], the use of this drug in treating human disease has grown to the point where it is now one of the most widely used antineoplastics. Cisplatin has an established role in the treatment of testicular, ovarian, bladder, germ cell, and head and neck carcinomas [2,3]. It also has an expanding role in treating small cell carcinoma of the lung, cervical cancer, gastrointestinal cancers, and breast cancer [3]. Despite the initial response of many tumors to this drug, the prognosis for patients with these diseases is often poor due to the eventual emergence of drug-resistant populations in the tumor. This chapter will consider our current knowledge about the biochemical mechanisms of resistance to cisplatin. Since numerous thorough reviews on the subject have recently appeared [4–11], an exhaustive coverage of the literature will not be attempted. The focus instead will be directed at the progress that has been made in the last several years, particularly with human cell models, and at the gaps in our knowledge about those mechanisms of resistance believed to be important.

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Andrews, P.A. (1994). Mechanisms of acquired resistance to cisplatin. In: Goldstein, L.J., Ozols, R.F. (eds) Anticancer Drug Resistance. Cancer Treatment and Research, vol 73. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2632-2_11

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  • DOI: https://doi.org/10.1007/978-1-4615-2632-2_11

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