The DOI matches its Crossref record; 178 of the 178 references it cites were found in a registry or an index.
Cell cycle, CDKs and cancer: a changing paradigm
Abstract
Tumour-associated cell cycle defects are often mediated by alterations in cyclin-dependent kinase (CDK) activity. Misregulated CDKs induce unscheduled proliferation as well as genomic and chromosomal instability. According to current models, mammalian CDKs are essential for driving each cell cycle phase, so therapeutic strategies that block CDK activity are unlikely to selectively target tumour cells. However, recent genetic evidence has revealed that, whereas CDK1 is required for the cell cycle, interphase CDKs are only essential for proliferation of specialized cells. Emerging evidence suggests that tumour cells may also require specific interphase CDKs for proliferation. Thus, selective CDK inhibition may provide therapeutic benefit against certain human neoplasias.
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“In contrast, the demonstration that inactivation of these genes can prevent oncogene-induced tumor development in mouse models reinforced the view that these enzymes might be suitable cancer-specific drug targets (65).”
From Targeting CDK4 and CDK6: From Discovery to Therapy (2016) · cites this paper as [65]
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Cites
1 retracted
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Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
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p21 is a universal inhibitor of cyclin kinases
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- Hanks, S. et al. Constitutional aneuploidy and cancer predisposition caused by biallelic mutations in BUB1B. Nature Genet. 36, 1159–1161 (2004). · DOI
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p21 in cancer: Intricate networks and multiple activities
Abbas, T., & Dutta, A. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2657 · Cited by 2,712
“CDK1, at least in some tissues, may be the crucial target of p21 in tumorigenesi”
BackgroundMonitoring Drug Target Engagement in Cells and Tissues Using the Cellular Thermal Shift Assay
Molina, D. M., Jafari, R., Ignatushchenko, M., Seki, T., Larsson, E. A., Dan, C., Sreekumar, L., Cao, Y., & Nordlund, P. (2013) · Science · doi:10.1126/science.1233606 · Cited by 2,261
Programmed Cell Death in Animal Development and Disease
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“Other examples include the elimination of cells in response to viral infection, unrepaired DNA damage, cellcycle perturbations, and fate and differentiation defects (Abrams et al., 1993; Rossel and Capecchi, 1999; Derry et al., 2001, Vousden and Prives, 2009; Malumbres and Barbacid, 2009; Koto et al., 2011).”
Finn, R. S., Crown, J. P., Lang, I., Boer, K., Bondarenko, I. M., Kulyk, S. O., Ettl, J., Patel, R., Pinter, T., Schmidt, M., et al. (2015) · The Lancet Oncology · doi:10.1016/s1470-2045(14)71159-3 · Cited by 1,900
Cell cycle proteins as promising targets in cancer therapy
Otto, T., & Siciński, P. (2017) · Nature reviews. Cancer · doi:10.1038/nrc.2016.138 · Cited by 1,931
“Chk1 is an essential kinase that is regulated by Atr and required for the G(2)/M DNA damage checkpoint.”
Metadata
- Authors
- Malumbres, M., & Barbacid, M.
- Affiliations
- Spanish National Cancer Research Centre (ES)
- Venue
- Nature Reviews Cancer
- Published
- 2009-03
- Volume
- 9
- Issue
- 3
- Pages
- 153-166
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- OpenAlex
- W2046024621
- Cited by
- 3,957
- References
- 178
- Citations by year
- 2026: 191 · 2025: 241 · 2024: 266 · 2023: 277 · 2022: 297 · 2021: 318 · 2020: 272 · 2019: 222 · 2018: 237 · 2017: 260 · 2016: 195 · 2015: 228 · 2014: 218 · 2013: 206 · 2012: 186
- FWCI
- 15.80
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- cyclin-dependent kinases, CDK1, cell cycle, tumor cell proliferation, genomic instability, chromosomal instability, cyclin-dependent kinase inhibitors, selective cancer therapy
- MeSH terms
- Animals, Cell Cycle, Chromosome Aberrations, DNA Damage, Humans, Mitosis, Neoplasms, Neoplastic Stem Cells, Cyclins, Cyclin-Dependent Kinases, Cyclin E, Chromosomal Instability, Protein Kinase Inhibitors, Cell Proliferation, Cyclin D
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