The DOI matches its Crossref record; 98 of the 98 references it cites were found in a registry or an index.
Cell-cycle checkpoints and cancer
Abstract
All life on earth must cope with constant exposure to DNA-damaging agents such as the Sun's radiation. Highly conserved DNA-repair and cell-cycle checkpoint pathways allow cells to deal with both endogenous and exogenous sources of DNA damage. How much an individual is exposed to these agents and how their cells respond to DNA damage are critical determinants of whether that individual will develop cancer. These cellular responses are also important for determining toxicities and responses to current cancer therapies, most of which target the DNA.
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“CHK1 prevents new origin firing by inhibiting CDK2 through CDC25A degradation, thus hindering the subsequent loading of CDC45 on chromatin to form the pre-initiation complex [34].”
From The Spi1/PU.1 transcription factor accelerates replication fork progression by increasing PP1 phosphatase in leukemia (2017) · cites this paper as [34]
In the citing paper
“The importance of the DNA damage checkpoint in the maintenance of genomic stability is underlined by the existence of many syndromes linked to mutations in checkpoint genes, causing increased cancer proneness or other clinical symptoms, especially neurological defects [13,14]”
From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [13]
In the citing paper
“while p53-mutant mice are cancer prone, we noted that their predilection for mesenchymal and lymphoid malignancies, rather than epithelial cancers, did not represent the tumor types most commonly possessing p53 mutations in humans (101,102).”
From Telomeres and telomerase in cancer (2010) · cites this paper as [101]
In the citing paper
“factors involved in DNA repair and DDR pathways have become therapeutic targets and are currently being tested in both laboratory and clinical studies [151, 222]”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [222]
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Canman, C. E. (2003) · Current Biology · doi:10.1016/s0960-9822(03)00410-x · Cited by 40
Loss of Rad52 partially rescues tumorigenesis and T-cell maturation in Atm-deficient mice
Treuner, K., Helton, R., & Barlow, C. (2004) · Oncogene · doi:10.1038/sj.onc.1207604 · Cited by 33
Flagged first, then by citations
Research works printed but not linked: 1
- Ford, J. M. Clinical Oncology (eds Abeloff, M. et al.) Ch. 11, 191–205 (Elsevier, Philadelphia, 2004).
Cited by
Sorted by citations
Glioma stem cells promote radioresistance by preferential activation of the DNA damage response
Bao, S., Wu, Q., McLendon, R. E., Hao, Y., Shi, Q., Hjelmeland, A. B., Dewhirst, M. W., Bigner, D. D., & Rich, J. N. (2006) · Nature · doi:10.1038/nature05236 · Cited by 6,517
The DNA-damage response in human biology and disease
Jackson, S. P., & Bartek, J. (2009) · Nature · doi:10.1038/nature08467 · Cited by 6,092
Cell cycle, CDKs and cancer: a changing paradigm
Malumbres, M., & Barbacid, M. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2602 · Cited by 3,957
ATM and ATR Substrate Analysis Reveals Extensive Protein Networks Responsive to DNA Damage
Matsuoka, S., Ballif, B. A., Smogorzewska, A., McDonald, E. R., Hurov, K. E., Luo, J., Bakalarski, C. E., Zhao, Z., Solimini, N., Lerenthal, Y., et al. (2007) · Science · doi:10.1126/science.1140321 · Cited by 3,075
DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis
Bartkova, J., Hořejší, Z., Koed, K., Krämer, A., Tort, F., Zieger, K., Guldberg, P., Sehested, M., Nesland, J. M., Lukas, C., et al. (2005) · Nature · doi:10.1038/nature03482 · Cited by 2,688
Metadata
- Authors
- Kastan, M. B., & Bartek, J.
- Affiliations
- St. Jude Children's Research Hospital (US)
- ORCID
- Kastan, Michael B.
- Venue
- Nature
- Published
- 2004-11
- Volume
- 432
- Issue
- 7015
- Pages
- 316-323
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W1965239527
- Cited by
- 2,836
- References
- 98
- Citations by year
- 2026: 61 · 2025: 71 · 2024: 70 · 2023: 111 · 2022: 132 · 2021: 151 · 2020: 144 · 2019: 119 · 2018: 114 · 2017: 130 · 2016: 141 · 2015: 138 · 2014: 151 · 2013: 141 · 2012: 164
- FWCI
- 9.07
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Keywords
- cell cycle checkpoints, DNA damage response, DNA repair, cancer, DNA-damaging agents, radiation, cancer therapy toxicity, carcinogenesis
- MeSH terms
- Animals, Cell Cycle, DNA Damage, Humans, Neoplasms, Signal Transduction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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