ArticleNucleic acids research2005
Inhibition of double-strand break non-homologous end-joining by cisplatin adducts in human cell extracts.
Article in Nucleic acids research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- Cell-cycle-specific lesion evolution rather than inhibition of double-strand-break repair underpins cisplatin radiosensitization.Molecular oncology · 2026Article
- Article
- Emerging and established therapies for chemotherapy-induced ototoxicity.Journal of cancer survivorship : research and practice · 2023Review
- Can Cisplatin Therapy Be Improved? Pathways That Can Be Targeted.International journal of molecular sciences · 2022Review
- Article
- The Role of Tumour Metabolism in Cisplatin Resistance.Frontiers in molecular biosciences · 2021Review
- The genome-wide sequence preference of ionising radiation-induced cleavage in human DNA.Molecular biology reports · 2019Article
- BRCA1 and BARD1 mediate apoptotic resistance but not longevity upon mitochondrial stress inEMBO reports · 2018Article
- Effects of electromagnetic field, cisplatin and morphine on cytotoxicity and expression levels of DNA repair genes.Molecular biology reports · 2018Article
- DNA damage repair in ovarian cancer: unlocking the heterogeneity.Journal of ovarian research · 2018Review
- A short time interval between radiotherapy and hyperthermia reduces in-field recurrence and mortality in women with advanced cervical cancer.Radiation oncology (London, England) · 2017Article
- Ovarian Cancers Harbor Defects in Nonhomologous End Joining Resulting in Resistance to Rucaparib.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- Sensitizing thermochemotherapy with a PARP1-inhibitor.Oncotarget · 2017Article
- DNA damage response (DDR) pathway engagement in cisplatin radiosensitization of non-small cell lung cancer.DNA repair · 2016Article
- Complex cisplatin-double strand break (DSB) lesions directly impair cellular non-homologous end-joining (NHEJ) independent of downstream damage response (DDR) pathways.The Journal of biological chemistry · 2012Article
- Current advances in DNA repair: regulation of enzymes and pathways involved in maintaining genomic stability.Antioxidants & redox signaling · 2011Article
- Marked anti-tumour activity of the combination of YM155, a novel survivin suppressant, and platinum-based drugs.British journal of cancer · 2010Article
- Small-scale extracts for the study of nucleotide excision repair and non-homologous end joining.Nucleic acids research · 2007Article
- Inhibition of homologous recombination repair with Pentoxifylline targets G2 cells generated by radiotherapy and induces major enhancements of the toxicity of cisplatin and melphalan given after irradiation.Radiation oncology (London, England) · 2006Review
- Differential and collaborative actions of Rad51 paralog proteins in cellular response to DNA damage.Nucleic acids research · 2005Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effect of cis-diaminedichloroplatinum(II) (cisplatin) DNA damage on the repair of double-strand breaks by non-homologous end-joining (NHEJ) was determined using cell-free extracts. NHEJ was dramatically decreased when plasmid DNA was damaged to contain multiple types of DNA adducts, along the molecule and at the termini, by incubation of DNA with cisplatin; this was a cisplatin concentration-dependent effect. We investigated the effect a single GTG cisplatination site starting 10 bp from the DNA termini would have when surrounded by the regions of AT-rich DNA which were devoid of the major adduct target sequences. Cisplatination of a substrate containing short terminal 13-15 bp AT-rich sequences reduced NHEJ to a greater extent than that of a substrate with longer (31-33 bp) AT-rich sequences. However, cisplatination at the single GTG site within the AT sequence had no significant effect on NHEJ, owing to the influence of additional minor monoadduct and dinucleotide adduct sites within the AT-rich region and owing to the influence of cisplatination at sites upstream of the AT-rich regions. We then studied the effect on NHEJ of one cis-[Pt(NH3)2{d(GpTpG)-N7(1),-N7(3)} [abbreviated as 1,3-d(GpTpG)] cisplatin adduct in the entire DNA molecule, which is more reflective of the situation in vivo during concurrent chemoradiation. The presence of a single 1,3-d(GpTpG) cisplatin adduct 10 bases from each of the two DNA ends to be joined resulted in a small (30%) but significant decrease in NHEJ efficiency. This process, which was DNA-dependent protein kinase and Ku dependent, may in part explain the radiosensitizing effect of cisplatin administered during concurrent chemoradiation.
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