Cell-cycle checkpoints and cancer
By M. Kastan, J. Bartek. Nature, 2004
2,945 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/ea86d05d3d6912d8bd8f296cec9d2f6c6e00f8e5
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
- J. Bartek
- Stephen P. Jackson
- Yves Pommier
- J. Lukas
- J. R. Chapman
- Jüergen Cox
- Jesper V. Olsen
- Marcos Malumbres
In Molecular Biology
- Matthias Mann
- J. Bartek
- Jüergen Cox
- Stephen P. Jackson
- J. Lukas
- Jesper V. Olsen
- Florian Gnad
- K. Guan
In Oncology
- Stephen P. Jackson
- J. Bartek
- J. Lukas
- Yves Pommier
- Marcos Malumbres
- Matthias Mann
- J. R. Chapman
- T. Halazonetis
Citations in the corpus
- Oxidative stress as a mediator of life history trade-offs: mechanisms, measurements and interpretation. (2009, background): “Repair of DNA is very important to cell function, and several complex damage recognition and repair pathways exist (Kastan & Bartek 2004).”
- DNA helicases Sgs1 and BLM promote DNA double-strand break resection. (2008, background): “The importance of such responses is revealed by the fact that inherited defects in them lead to human pathologies, including cancer, infertility and neurodegeneration (Khanna and Jackson 2001; Kastan and Bartek 2004).”
- p53-deficient cells rely on ATM- and ATR-mediated checkpoint signaling through the p38MAPK/MK2 pathway for survival after DNA damage. (2007, background): “Disruption of normal checkpoint function from inherited and acquired genetic mutations is increasingly recognized as a pathophysiological mechanism responsible for tumor-prone human disease syndromes (Bartek and Lukas, 2003; Kastan and Bartek, 2004; O'Driscoll et al., 2004; Shiloh, 2003).”
- Quantitative Phosphoproteomics Reveals Widespread Full Phosphorylation Site Occupancy During Mitosis (2010, background): “Progression through the cell cycle is governed by a complex network of regulatory proteins and signaling pathways, and deregulation of key players that coordinate this process can lead to carcinogenesis (1, 2).”
- The molecular biology of head and neck cancer (2011, background): “One of the key cellular functions that is often, if not always, changed in cancer cells to overcome senescence and to obtain limitless replicative potential is the regulation of the cell cycl”
- Cell cycle, CDKs and cancer: a changing paradigm (2009, background): “In addition, most tumours acquire genomic instability (GIN) that leads to additional mutations as well as chromosomal instability (CIN), a defect responsible for numerical changes in chromosome”
- Computational assignment of cell-cycle stage from single-cell transcriptome data. (2015, neutral): “Moreover, the cell cycle is known to be linked to fundamental biological processes, including cell differentiation [7] and oncogenesis [8,9].”
- Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions (2005, positive): “dtd" [ ]> DNA damage checkpoint genes, such as p53 , are frequently mutated in human cancer, but the selective pressure for their inactivation remains elusiv”