The DNA damage response and cancer therapy

By C. Lord, Alan Ashworth. Nature, 2012

1,734 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/2a47e7027a374ae59d0513bc92afee7a343c760d

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In Oncology

Citations in the corpus

TITAN: inference of copy number architectures in clonal cell populations from tumor whole-genome sequence data (2014, background): “Tumors exhibiting subclonal CNA and LOH events are likely to have acquired HR defects and would be good candidates for treatment with platinum-based drugs or PARP inhibitors (Mukhopadhyay et al. 2012; Wang et al. 2012).”
ROS and the DNA damage response in cancer (2018, background): “The response to DSBs is particularly relevant in carcinogenesis and cancer therapy, as many of the components of the pathway are mutated in cancer, and most current cancer treatment (chemotherapy and radiotherapy) exploits these defects [8].”
Regulation of ligands for the NKG2D activating receptor (2013, background): “The replication stress itself, as well as the resulting DNA breaks, are each thought to independently activate the DNA damage response, a protein kinase cascade that regulates numerous aspects of cell physiology (36).”
DNA damage repair: historical perspectives, mechanistic pathways and clinical translation for targeted cancer therapy (2021, background): “To date, a large number of DDR genes have been identified in various cancers.(150,151) Figure 3 illustrates the timeline of DDR-related findings and concepts related to cancer, highlighting the scientists who worked to provide a deeper understanding of the roles of DDR in cancer.”
Nanomedicine therapeutic approaches to overcome cancer drug resistance (2013, background): “These mechanisms are used to prevent the transmission of damaged DNA and to avoid malignant transformation [29].”
Stereospecific PARP trapping by BMN 673 and comparison with olaparib and rucaparib (2013, background): “Since the discovery of the synthetic lethality of PARP inhibitors in homologous recombination–deficient cells (15, 18–23), the mechanism by which PARP inhibitors exert their cytotoxicity has been dominantly interpreted as an accumulation of unrepaired SSBs resulting from catalytic PARP inhibition (7”
Ageing as a risk factor for disease. (2012, background): “In cancer cells, DDR pathway components, such as ATM and BRCA1, have to be impaired for a tumour to develop [97], allowing cells to proliferate regardless of their damaged DNA, and without repairing it, which leads to further DNA damage and, eventually, to a highly proliferating and mutagenized cell”
HRDetect is a predictor of BRCA1 and BRCA2 deficiency based on mutational-signatures (2017, background): “%) who could have selective therapeutic sensitivity to PARP inhibition. and BRCA2 proteins have multiple, distinct roles in maintaining genome integrity, particularly through homologous recombination (HR)-mediated double-strand break (DSB) repair 6 .”
Spatial and temporal diversity in genomic instability processes defines lung cancer evolution (2014, background): “Evidence for spatial diversity in genomic instability processes suggests that opportunities to exploit such mechanisms therapeutically may be limited in this disease(33).”
The hallmarks of aging. (2013, background): “…well as of other chromatin-associated proteins, can induce epigenetic changes that contribute to the aging process. organisms have evolved a complex network of DNA repairmechanisms that are collectively capable of dealing with most of the damages inflicted to nuclear DNA (Lord and Ashworth, 2012).”