Cisplatin: mode of cytotoxic action and molecular basis of resistance

By Z. Siddik. Oncogene, 2003

3,308 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/b2156e163ea2fcf2f558210307d645c5f88d3066

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. Guido Kroemer
2. L. Galluzzi
3. Oliver Kepp
4. C. Brenner
5. S. Alexander
6. Hannah Alexander
7. A. Mesika
8. J. Min

In Oncology

1. Guido Kroemer
2. L. Galluzzi
3. Oliver Kepp
4. Matthew D. Hall
5. Lynn M. Pouliot
6. D. Shen
7. M. Dolan
8. D. Stewart

Citations in the corpus

• (Dihydro)ceramide Synthase 1–Regulated Sensitivity to Cisplatin Is Associated with the Activation of p38 Mitogen-Activated Protein Kinase and Is Abrogated by Sphingosine Kinase 1 (2007, background): “are far from having a full understanding of all the relevant signaling pathways involved (2).”
• Systems biology of cisplatin resistance: past, present and future (2014, background): “as well as in the machinery that de facto executes cell death.(12,48,154) Malignant cells are (i) intrinsically more resistant to adverse microenvironmental and intracellular cues than their non-transformed counterparts(155,156) and (ii) highly prone to acquire additional genetic and epigenetic alte”
• Pathophysiology of Cisplatin-Induced Acute Kidney Injury (2014, background): “Pathophysiological pathways implicated in cisplatin-induced AKI and their in vivo therapeutic models and molecules are presented in Table 2.”
• Molecular mechanisms of cisplatin resistance (2012, background): “The detailed description of the molecular mechanisms that underlie the anticancer potential of cisplatin goes largely beyond the scope of this review, and can be found elsewhere (Kelman and Peresie, 1979; Sanderson et al., 1996; Siddik, 2003).”
• Mechanisms of resistance to cisplatin and carboplatin. (2007, background): “Caspases 3, 8, and 9 are important in cisplatin-induced poptosis [53].”
• Cisplatin nephrotoxicity: mechanisms and renoprotective strategies. (2008, background): “First, once in a cell, cisplatin is aquated into a highly reactive form, which can rapidly react with thiol-containing molecules including glutathinone, a well-recognized cellular antioxidant.(4,5)”
• Molecular mechanisms of drug resistance (2005, neutral): “in regulating platinum drug resistance [24].”
• Colorectal Carcinoma: A General Overview and Future Perspectives in Colorectal Cancer (2017, background): “An increase in cytosolic drug inactivation and a reduction in drug uptake are other possibilities [277,278].”
• Cisplatin in cancer therapy: molecular mechanisms of action (2014, neutral): “The cytotoxic effect is likely a result of inhibition of replication by cisplatin-DNA adducts and induction of apoptosis (Siddik, 2003).”
• Molecular mechanisms of resistance and toxicity associated with platinating agents. (2007, background): “Increased concentrations of these compounds are known to induce resistance against cisplatin (Figure 3, Table 2) (reviewed in [16]).”
• Cisplatin Resistance: A Cellular Self-Defense Mechanism Resulting from Multiple Epigenetic and Genetic Changes (2012, background): “The cytotoxic lesions caused by platinating agents are known as platinum-DNA adducts, which primarily form intrastrand cross-links that activate the apoptotic pathway, resulting in cell death (Siddik, 2003).”