Mechanisms of resistance to cisplatin.

By M. Kartalou, J. Essigmann. Mutation research, 2001

862 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/b075527693d9f727bff5bd9e597b4486b67ad8e9

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. Sumit Ghosh
2. M. Dolan
3. J. Shim
4. Minoru Yoshida
5. Bowen Du
6. C. Rabik

In Oncology

1. M. Dolan
2. J. Shim
3. Sumit Ghosh
4. Bowen Du
5. C. Rabik

Citations in the corpus

• Copper complexes as anticancer agents. (2009, background): “The combined interest in (i) improving the DNA cleavage specificity of (52) type complexes together with their ability to perform double-strand breaks (DSB) and (ii) circumventing drug resistance owing to the use of cisplatin [190-194] inspired the design of bifunctional molecules (53a) and (53b) [1”
• Molecular mechanisms of resistance and toxicity associated with platinating agents. (2007, background): “Treatment with cisplatin or carboplatin results in the activation of complex signaling cascades in the cell [2].”
• Cisplatin: The first metal based anticancer drug. (2019, background): “It is well established that alterations expression of oncogenes like c-fos, Hras, c-abl and c-myc and tumor suppressor gene like p53 can create cellular resistance to cisplatin [86].”
• Targeting Epithelial–Mesenchymal Transition (EMT) to Overcome Drug Resistance in Cancer (2016, background): “Drug resistance (or chemoresistance) can be divided into two groups: intrinsic (or de novo) drug resistance and acquired drug resistance [2,3].”
• Cisplatin as an Anti-Tumor Drug: Cellular Mechanisms of Activity, Drug Resistance and Induced Side Effects (2011, background): “While the knowledge of the mechanism of action of CDDP has improved our understanding of resistance [70], the mechanism of decreased intracellular accumulation of CDDP is not well understood.”
• FK228 (depsipeptide) as a natural prodrug that inhibits class I histone deacetylases. (2002, background): “For instance, conjugation of cisplatin with glutathione inhibits the conversion of monoadducts to cross-links, thereby reducing the cytotoxic potential of the adducts (32).”