Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints

By J. Bártková, Nousin Rezaei, M. Liontos, Panagiotis Karakaidos, D. Kletsas, N. Issaeva, L. Vassiliou, E. Kolettas, Katerina Niforou, V. Zoumpourlis and 15 more. Nature, 2006

2,043 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Physiology

View Paper: https://www.semanticscholar.org/paper/cbb5a50b3176336ca331dcc6310fbe3e2ac387dc

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In Molecular Biology

1. J. Campisi
2. Jesús Gil
3. Adam Freund
4. F. Rodier
5. D. Meek
6. Manuel Serrano
7. D. Peeper
8. T. Kuilman

In Oncology

1. J. Campisi
2. Jesús Gil
3. Stephen J. Elledge
4. Marcos Malumbres
5. D. Meek
6. C. Lord
7. Ji Luo
8. N. Solimini

In Physiology

1. J. Campisi
2. Jesús Gil
3. Adam Freund
4. Manuel Serrano
5. F. Rodier
6. D. Peeper
7. T. Kuilman
8. M. Demaria

Citations in the corpus

• DNA replication stress as a hallmark of cancer. (2015, methodology): “Other oncogenes, such as RAS and MOS, which induce DNA replication stress, also enhance Cdc6 protein levels, and ectopic expression of Cdc6 is sufficient to induce DNA replication stress (63).”
• 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”
• Genomic instability — an evolving hallmark of cancer (2010, background): “The first is the mutator hypothesis described above and the second is the oncogene-induced DNA replication stress model for cancer developmen”
• Nucleotide Deficiency Promotes Genomic Instability in Early Stages of Cancer Development (2011, positive): “More recently, genomic instability in early cancer stages was shown to be caused by stress on the DNA replication, conferred by oncogene expression (Bartkova et al., 2006; Di Micco et al., 2006).”
• Four faces of cellular senescence (2011, positive): “DNA-SCARS include dysfunctional telomeres or telomere dysfunction–induced foci (TIF; d’Adda di Fagagna et al., 2003; Takai et al., 2003; Herbig et al., 2004; Kim et al., 2004). replication fork collapse (Bartkova et al., 2006; Di Micco et al., 2006; Mallette et al., 2007).”
• Senescence impairs successful reprogramming to pluripotent stem cells. (2009, background): “It has been shown that constitutively active HRAS leads to DNA replication stress that might result from impaired or inappropriately activated origins of replication, a phenomenon known as hyperreplication (Bartkova et al., 2006; Di Micco et al., 2006; Malletle et al., 2007).”
• Persistent DNA damage signaling triggers senescence-associated inflammatory cytokine secretion (2009, background): “but undergo OIS depending on the oncogene and contex”
• Senescence of activated stellate cells limits liver fibrosis (2008, background): “Of note, Rae family proteins, the NKG2D ligands in mice, are upregulated in response to DNA damage (Gasser et al., 2005), which also is a trigger for cellular senescence (Bartkova et al., 2006; Di Micco et al., 2006; Mallette et al., 2007).”