Cisplatin is a potent cytostatic frequently used in the treatment of malignant tumors. The main mechanism of antitumor effect of cisplatin is the interaction with DNA and the covalent link of cytostatic to the purine bases, mainly guanine.
This article summarizes current knowledge about a molecular response of the cells to cisplatin treatment; focuses on a DNA repair by nucleotide excision repair and mismatch repair, an apoptosis induction, a role of p53, and a role of checkpoint kinases and mitogen activated protein kinases.