DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis

By J. Bártková, Z. Hořejší, K. Koed, A. Krämer, F. Tort, K. Zieger, P. Guldberg, M. Sehested, J. Nesland, C. Lukas and 3 more. Nature, 2005

2,799 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/94175dcb0b26762d24c95ba660fec59a79022df2

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Citations in the corpus

Targeting mutant p53 for efficient cancer therapy (2017, methodology): “Stictic acid Modelling 1,4-Dihydroxy-10methoxy-5,8-dimethyl3,7-dioxo-1,3-dihydro7H-2,6,12-trioxabenzo [5,6]cyclohepta[1,2-e] indene-11-carbaldehyde Binds p53 in silico Experimental and/or preclinical 2013 68”
Modeling the therapeutic efficacy of p53 restoration in tumors. (2006, background): “Finally, persistent DNA damage is reported to be a frequent feature in human cancers from their earliest stages, possibly due to deregulated DNA replication (Bartkova et al., 2005; Gorgoulis et al., 2005).”
DNA damage repair: historical perspectives, mechanistic pathways and clinical translation for targeted cancer therapy (2021, background): “In 2005, DDR was described as an anticancer barrier in early-stage tumorigenesis, but the genes showing DDR mutations were absent from later-stage tumors.(149) To date, a large number of DDR genes have been identified in various cancers.”
Nucleotide Deficiency Promotes Genomic Instability in Early Stages of Cancer Development (2011, background): “Previous studies have demonstrated that, in early stages of cancer development, the instability occurs preferentially in genomic regions that are sensitive to replication stress, defined as fragile sites (Bartkova et al., 2005; Di Micco et al., 2006; Gorgoulis et al., 2005; Tsantoulis et al., 2008).”
RNF8 transduces the DNA-damage signal via histone ubiquitylation and checkpoint protein assembly. (2007, background): “Mutations in a variety of components involved in these C cellular processes directly contribute to tumorigenesis (Bartkova et al., 2005; Gorgoulis et al., 2005), highlighting the importance of these damage-induced signaling cascades in tumor suppression.”
Cancer metastasis: building a framework. (2006, background): “Damage to genomic DNA is evident even in apparently normal cells and becomes amplified as tumors emerge (Bartkova et al., 2005; Feinberg et al., 2006; Gorgoulis et al., 2005).”
Autophagy mitigates metabolic stress and genome damage in mammary tumorigenesis. (2007, background): “Limiting ATP levels and/or direct DNA insult by ROS may cause replication stress and DNA damage response activation, which normally arrests cell cycle progression or triggers apoptosis, and can therefore act as a barrier to early carcinogenesis (Bartkova et al. 2005; Gorgoulis et al. 2005).”
RAS oncogenes: weaving a tumorigenic web (2011, background): “An inevitable consequence of the persistent mitogenic stimulation that is imposed by RAS is the initiation of replicative stress, which is marked by increased numbers of active DNA replication origins and collapsed replication forks, which ultimately leads to DNA damage and the activation of the DN”
Regulation of ligands for the NKG2D activating receptor (2013, background): “Poorly regulated DNA replication (termed replication stress), characterized by collapsed replication forks, can result in DNA breaks (34, 35).”
DeepTox: Toxicity Prediction using Deep Learning (2016, background): “…relevant to human health, since activation of nuclear receptors can disrupt endocrine system function (Chawla et al., 2001; Grün and Blumberg, 2007), and activation of stress response pathways can lead to liver injury or cancer (Bartkova et al., 2005; Labbe et al., 2008; Jaeschke et al., 2012).”
Cell cycle, CDKs and cancer: a changing paradigm (2009, background): “In addition, recent studies have proposed that the DNA damage response may act as an anticancer barrie”
53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress (2011, neutral): “Finally, one aspect of our results is potentially relevant to the recent concept of replication stress acting as an inducer of biological barriers against tumour progressio”