Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions

By Vassilis G. Gorgoulis, L. Vassiliou, Panagiotis Karakaidos, Panayotis Zacharatos, A. Kotsinas, T. Liloglou, M. Venere, Richard A. DiTullio, N. Kastrinakis, B. Levy and 5 more. Nature, 2005

2,107 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/862935011d05593c96f9feac523892069a51c87f

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. J. Campisi
2. Stephen J. Elledge
3. Stephen P. Jackson
4. J. Bartek
5. J. Lukas
6. Ji Luo
7. N. Solimini
8. Junjie Chen

In Molecular Biology

1. J. Campisi
2. Stephen P. Jackson
3. J. Bartek
4. J. Lukas
5. F. Rodier
6. Stephen J. Elledge
7. J. Massagué
8. Andrew N. Blackford

In Oncology

1. Stephen P. Jackson
2. J. Bartek
3. Stephen J. Elledge
4. J. Lukas
5. Ji Luo
6. N. Solimini
7. J. Campisi
8. J. Massagué

Citations in the corpus

• Nucleotide Deficiency Promotes Genomic Instability in Early Stages of Cancer Development (2011, positive): “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).”
• 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).”
• DNA damage checkpoints: from initiation to recovery or adaptation. (2007, background): “Current Opinion in Cell Biology 2007, 19:238–245 cells with acquired defects in the DDR network (Figure 3), but also because it suggests potential therapeutic implications [17 ,56 ,63].”
• ATM, ATR, and DNA-PK: The Trinity at the Heart of the DNA Damage Response. (2017, background): “Small molecule inhibitors of ATM, ATR and DNA-PK as potential therapeutic agents As the DDR can be activated at early stages in tumorigenesis due to oncogene-induced replication stress or processes such as telomere shortening, this has suggested that cell-cycle arrest or cell death enforced by PIKK ”