1993
DOI: 10.1097/00001813-199308000-00011
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Evidence of differential cisplatin-DNA adduct formation, removal and tolerance of DNA damage in three human lung carcinoma cell lines

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Cited by 55 publications
(31 citation statements)
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“…Tyrosine kinase inhibitors (TKIs) are also frequently used, but platinum-based therapy remains the best option for the treatment of advanced NSCLC when the mutation status of the epidermal growth factor receptor (EGFR) is unknown (Bidoli et al, 2007;Jemal et al, 2009;Vilmar and Sørensen, 2009;National Comprehensive Cancer Network, 2011). However, the development of platinum-based therapies has slowed and many NSCLC patients derived little therapeutic benefit from any of those currently available (Shellard et al, 1993;Pfister et al, 2004;Wang et al, 2011). Seeking an optimal prognostic biomarker for clinical efficacy of platinum-based treatment remains a hotspot in this field.…”
Section: Introductionmentioning
confidence: 99%
“…Tyrosine kinase inhibitors (TKIs) are also frequently used, but platinum-based therapy remains the best option for the treatment of advanced NSCLC when the mutation status of the epidermal growth factor receptor (EGFR) is unknown (Bidoli et al, 2007;Jemal et al, 2009;Vilmar and Sørensen, 2009;National Comprehensive Cancer Network, 2011). However, the development of platinum-based therapies has slowed and many NSCLC patients derived little therapeutic benefit from any of those currently available (Shellard et al, 1993;Pfister et al, 2004;Wang et al, 2011). Seeking an optimal prognostic biomarker for clinical efficacy of platinum-based treatment remains a hotspot in this field.…”
Section: Introductionmentioning
confidence: 99%
“…Platinum causes platinum-DNA adducts that block transcription, leading to cytotoxicity and cell death, whereas increased removal of platinum from cancer cells and repair of platinum-DNA adducts by tolerance mechanisms induce drug resistance. 1 Therefore, efficient DNA repair can modulate platinum cytotoxicity and its anticancer efficacy. [2][3][4][5] Among DNA repair pathways, nucleotide excision repair (NER) is an important mechanism underlying cisplatin resistance by removing platinum-DNA interstrand adducts.…”
Section: Introductionmentioning
confidence: 99%
“…The development of resistance to cisplatin at a cellular level is believed to be a major obstacle to improving the outcome with cisplatin-based chemotherapy. Experimental models of cisplatin resistance have implicated multiple mechanisms including decreased drug accumulation, elevated glutathione and metallothionein levels, increased DNA repair and increased tolerance of DNA damage (Andrews and Howell, 1990;Shellard et al, 1993).…”
mentioning
confidence: 99%