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Platinum drugs and taxanes: can we overcome resistance?

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CELL DEATH DISCOVERY
卷 7, 期 1, 页码 -

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SPRINGERNATURE
DOI: 10.1038/s41420-021-00554-5

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资金

  1. Russian Ministry of Science and Education [075-15-2020-789]
  2. Russian Science Foundation [19-15-00125]
  3. Russian Foundation for Basic Research [18-29-09005, 20-015-00157]
  4. Stockholm Cancer Society [181301]
  5. Swedish Cancer Society [190345]

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Cancer therapy aims to eliminate tumor cells by targeting cell proliferation and inducing cell death. While apoptosis is commonly associated with anticancer drugs, other mechanisms of cell death, such as necroptosis and ferroptosis, may also play a significant role in determining the fate of cancer cells. Understanding the molecular crosstalk between different cell death pathways is crucial for the success of therapeutic interventions in cancer treatment.
Cancer therapy is aimed at the elimination of tumor cells and acts via the cessation of cell proliferation and induction of cell death. Many research publications discussing the mechanisms of anticancer drugs use the terms cell death and apoptosis interchangeably, given that apoptotic pathways are the most common components of the action of targeted and cytotoxic compounds. However, there is sound evidence suggesting that other mechanisms of drug-induced cell death, such as necroptosis, ferroptosis, autophagy, etc. may significantly contribute to the fate of cancer cells. Molecular cross-talks between apoptotic and nonapoptotic death pathways underlie the successes and the failures of therapeutic interventions. Here we discuss the nuances of the antitumor action of two groups of the widely used anticancer drugs, i.e., platinum salts and taxane derivatives. The available data suggest that intelligent interference with the choice of cell death pathways may open novel opportunities for cancer treatment.

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