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]
Citations
Cites
1 retracted
Fasano, C. A., Dimos, J. T., Ivanova, N. B., Lowry, N. A., Lemischka, I. R., & Temple, S. (2007) · Cell stem cell · doi:10.1016/j.stem.2007.04.001 · Cited by 308
RetractedTargeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy
Farmer, H., McCabe, N., Lord, C. J., Tutt, A. N. J., Johnson, D. A., Richardson, T. B., Santarosa, M., Dillon, K. J., Hickson, I., Knights, C., et al. (2005) · Nature · doi:10.1038/nature03445 · Cited by 6,683
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218
Lane, D. P. (1992) · Nature · doi:10.1038/358015a0 · Cited by 5,138
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649
p21 is a universal inhibitor of cyclin kinases
Xiong, Y., Hannon, G., Zhang, H., Casso, D., Kobayashi, R., & Beach, D. (1993) · Nature · doi:10.1038/366701a0 · Cited by 3,691
A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4.
Serrano, M., Hannon, G. J., & Beach, D. (1993) · Nature · doi:10.1038/366704a0 · Cited by 3,650
Patterns of somatic mutation in human cancer genomes
Greenman, C. D., Stephens, P., Smith, R., Dalgliesh, G. L., Hunter, C., Bignell, G. R., Davies, H. R., Teague, J. W., Butler, A. P., Stevens, C., et al. (2007) · Nature · doi:10.1038/nature05610 · Cited by 3,143
Kastan, M. B., Zhan, Q., El-Deiry, W. S., Carrier, F., Jacks, T., Walsh, W. V., Plunkett, B. S., Vogelstein, B., & Fornace, A. J. (1992) · Cell · doi:10.1016/0092-8674(92)90593-2 · Cited by 3,047
Cell-cycle checkpoints and cancer
Kastan, M. B., & Bartek, J. (2004) · Nature · doi:10.1038/nature03097 · Cited by 2,836
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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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Consequence of the tumor-associated conversion to cyclin D1b
Augello, M. A., Berman‐Booty, L. D., Carr, R., Yoshida, A., Dean, J. L., Schiewer, M. J., Feng, F. Y., Tomlins, S. A., Gao, E., Koch, W. J., et al. (2015) · EMBO Molecular Medicine · doi:10.15252/emmm.201404242 · Cited by 23
“…by direct binding and activation of CDK4/6 complexes (Musgrove et al, 2011; Malumbres & Barbacid, 2009). cyclin D1/CDK4/6 subsequently phosphorylates key substrates (including the retinoblastoma tumor suppressor, RB) which induces progression from G1 to S phase (Malumbres & Barbacid, 2009).”
BackgroundInfluentialA high-content cellular senescence screen identifies candidate tumor suppressors, including EPHA3
Lahtela, J., Corson, L. B., Hemmes, A., Brauer, M. J., Koopal, S., Lee, J., Hunsaker, T. L., Jackson, P. K., & Verschuren, E. W. (2013) · Cell Cycle · doi:10.4161/cc.23515 · Cited by 20
Romero-Benavides, J. C., Bailon-Moscoso, N., Parra-Delgado, H., Ramirez, M. I., Villacis, J., Cabrera, H., Gonzalez-Arevalo, G., Cueva, R., Zentella-Dehesa, A., Ratovitski, E. A., et al. (2018) · Medicinal Chemistry Research · doi:10.1007/s00044-017-2106-4 · Cited by 17
“6a. Mammalian cell cycle consists an ordered set of events, named as G1, S, G2, and mitotic phase, which include cell growth, DNA replication, distribution of the duplicated chromosomes to daughter cells, and cell division, respectively (Malumbres and Barbacid 2009).”
BackgroundResistance Mechanisms to Cyclin-Dependent Kinase Inhibitors
Wiedemeyer, W. R. (2018) · Resistance to Targeted Anti-Cancer Therapeutics · doi:10.1007/978-3-319-67932-7_8 · Cited by 7
Computational challenges of cell cycle analysis using single cell transcriptomics
Chervov, A., & Zinovyev, A. (2022) · arXiv · doi:10.48550/arxiv.2208.05229 · Cited by 4
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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