Molecular mechanisms of cisplatin resistance

By L. Galluzzi, L. Senovilla, I. Vitale, J. Michels, Isabelle Martins, Oliver Kepp, M. Castedo, Guido Kroemer. Oncogene, 2012

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Systems biology of cisplatin resistance: past, present and future (2014, background): “CDDP-elicited DNA adducts can engender double-strand breaks (DSBs), which are normally repaired along with DNA synthesis (or shortly after) via homologous recombination (HR).136 Accordingly, HR-deficient neoplasms, such as those bearing loss-of-function mutations in the genes encoding breast cancer ”
Glutaminolysis: A Hallmark of Cancer Metabolism. (2017, background): “CAFs: cancer-associated fibroblasts and induces apoptosis (Figure 7a) (107, 108).”
Cisplatin: The first metal based anticancer drug. (2019, background): “The detail for mechanism of cisplatin resistance remains elsewhere [99].”
Nrf2 inhibition reverses the resistance of cisplatin-resistant head and neck cancer cells to artesunate-induced ferroptosis (2016, background): “However, cisplatin is commonly associated with acquired resistance and the toxicity of various organs in clinical settings, which leads to a failure in cancer patient management [6].”
Mitochondrial metabolism and cancer (2017, background): “Mitochondria are critically involved in the control of RCD triggered by all these treatments, implying that alterations of the propensity of mitochondria to undergo MOMP or MPT underlie a majority of cases of primary and acquired resistance [163-166].”