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Co-inhibition of Pol η and ATR sensitizes cisplatin-resistant non-small cell lung cancer cells to cisplatin by impeding DNA damage repair.
In this study, we showed that there was no difference in intracellular uptake of cisplatin or the removal of platinum-DNA adducts between a cisplatin-resistant NSCLC cell line (A549/DR) and a cisplatin-sensitive NSCLC cell line (A549). However, the capacity to repair DNA interstrand crosslinks (ICLs) and double-strand breaks (DSBs) was significantly enhanced in the A549/DR cell line compared to 3 cisplatin-sensitive cell lines. We found that the protein and mRNA expression levels of Pol η, a Y-family translesion synthesis (TLS) polymerase, were markedly increased upon cisplatin exposure in A549/DR cells compared with A549...
Source: Acta Pharmacologica Sinica - May 31, 2018 Category: Drugs & Pharmacology Authors: Li XQ, Ren J, Chen P, Chen YJ, Wu M, Wu Y, Chen K, Li J Tags: Acta Pharmacol Sin Source Type: research

The catalytic topoisomerase II inhibitor dexrazoxane induces DNA breaks, ATF3 and the DNA damage response in cancer cells
Conclusions and ImplicationsSimilar to TOP2A poisons, DRZ induces DNA double‐strand breaks followed by activation of DNA damage response. The DNA damage‐triggered ATF3 controls the level of p53 accumulation as well as double‐strand breaks generation and is proposed to serve as a switch between DNA damage and cell death following DRZ treatment. These findings suggest a mechanistic explanation for the diverse clinical observations associated with DRZ.
Source: British Journal of Pharmacology - December 17, 2014 Category: Drugs & Pharmacology Authors: Shiwei Deng, Tiandong Yan, Teodora Nikolova, Dominik Fuhrmann, Andrea Nemecek, Ute Gödtel‐Armbrust, Bernd Kaina, Leszek Wojnowski Tags: Research Paper Source Type: research