The DOI matches its Crossref record; 56 of the 56 references it cites were found in a registry or an index.
The Requirement for Cyclin D Function in Tumor Maintenance
Open accessAbstract
D-cyclins represent components of cell cycle machinery. To test the efficacy of targeting D-cyclins in cancer treatment, we engineered mouse strains that allow acute and global ablation of individual D-cyclins in a living animal. Ubiquitous shutdown of cyclin D1 or inhibition of cyclin D-associated kinase activity in mice bearing ErbB2-driven mammary carcinomas triggered tumor cell senescence, without compromising the animals' health. Ablation of cyclin D3 in mice bearing Notch1-driven T cell acute lymphoblastic leukemias (T-ALL) triggered tumor cell apoptosis. Such selective killing of leukemic cells can also be achieved by inhibiting cyclin D associated kinase activity in mouse and human T-ALL models. Inhibition of cyclin D-kinase activity represents a highly-selective anticancer strategy that specifically targets cancer cells without significantly affecting normal tissues.
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“Depending on the cell type and the transforming event, some Rb-positive cells undergo quiescence and others undergo senescence when treated with CDK4/6 inhibitors (Baughn et al., 2006; Choi et al., 2012; Kovatcheva et al., 2015; Michaud et al., 2010; Puyol et al., 2010).”
From CDK4/6 Inhibitors: The Mechanism of Action May Not Be as Simple as Once Thought (2018) · cites this paper as Choi et al., 2012
In the citing paper
“In T-cell acute lymphoblastic leukemia (T-ALL), inhibition of CDK6 or genetic repression of cyclin D3 induces apoptosis (Choi et al., 2012; Sawai et al., 2012).”
From CDK4/6 Inhibitors: The Mechanism of Action May Not Be as Simple as Once Thought (2018) · cites this paper as Choi et al., 2012
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Cites
The landscape of somatic copy-number alteration across human cancers
Beroukhim, R., Mermel, C. H., Porter, D., Wei, G., Raychaudhuri, S., Donovan, J., Barretina, J., Boehm, J. S., Dobson, J., Urashima, M., et al. (2010) · Nature · doi:10.1038/nature08822 · Cited by 4,017
Self-citationCell cycle, CDKs and cancer: a changing paradigm
Malumbres, M., & Barbacid, M. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2602 · Cited by 3,957 · cited 1×
“CyclinCDK complexes phosphorylate cellular proteins, thereby driving cell cycle progression (Malumbres and Barbacid, 2009).”
BackgroundModel-based analysis of oligonucleotide arrays: Expression index computation and outlier detection.
Li, C., & Wong, W. H. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.98.1.31 · Cited by 3,133
Activating Mutations of NOTCH1 in Human T Cell Acute Lymphoblastic Leukemia
Weng, A. P., Ferrando, A. A., Lee, W., Morris, J. P., Silverman, L. B., Sanchez-Irizarry, C., Blacklow, S. C., Look, A. T., & Aster, J. C. (2004) · Science · doi:10.1126/science.1102160 · Cited by 2,706
Self-citationRb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence
Narita, M., Nuñez, S., Heard, E., Narita, M., Lin, A. W., Hearn, S. A., Spector, D. L., Hannon, G. J., & Lowe, S. W. (2003) · Cell · doi:10.1016/s0092-8674(03)00401-x · Cited by 2,278 · cited 1×
“Hypophosphorylated (active) pRB protein was shown to enforce the senescent state by permanently silencing expression of E2F target genes, such as cyclin E1, cyclin A2 or Dhfr (Chicas et al., 2010; Narita et al., 2003; Dean et al., 2010).”
BackgroundInducible Gene Targeting in Mice
Kühn, R., Schwenk, F., Aguet, M., & Rajewsky, K. (1995) · Science · doi:10.1126/science.7660125 · Cited by 1,641
Cyclin D as a therapeutic target in cancer
Musgrove, E. A., Caldon, C. E., Barraclough, J., Stone, A., & Sutherland, R. L. (2011) · Nature Reviews Cancer · doi:10.1038/nrc3090 · Cited by 1,370
Hayashi, S., & McMahon, A. P. (2002) · Developmental Biology · doi:10.1006/dbio.2002.0597 · Cited by 1,351
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“As soon as breast tumors were detected, we started treating mice with PD 0332991, a specific and potent inhibitor of cyclin D-CDK4 and D-CDK6 kinases (Fry et al., 2004).”
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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
The history and future of targeting cyclin-dependent kinases in cancer therapy
Asghar, U., Witkiewicz, A. K., Turner, N. C., & Knudsen, E. S. (2015) · Nature Reviews Drug Discovery · doi:10.1038/nrd4504 · Cited by 1,767
Small molecules in targeted cancer therapy: advances, challenges, and future perspectives
Zhong, L., Li, Y., Xiong, L., Wang, W., Wu, M., Yuan, T., Yang, W. M., Tian, C., Miao, Z., Wang, T., et al. (2021) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-021-00572-w · Cited by 1,813
CDK4/6 inhibition triggers anti-tumour immunity
Goel, S., DeCristo, M. J., Watt, A. C., BrinJones, H., Sceneay, J., Li, B. B., Khan, N., Ubellacker, J. M., Xie, S., Metzger-Filho, O., et al. (2017) · Nature · doi:10.1038/nature23465 · Cited by 1,513
Treating cancer with selective CDK4/6 inhibitors
O'Leary, B., Finn, R. S., & Turner, N. C. (2016) · Nature Reviews Clinical Oncology · doi:10.1038/nrclinonc.2016.26 · Cited by 1,137
Metadata
- Authors
- Choi, Y. J., Li, X., Hydbring, P., Sanda, T., Stefano, J., Christie, A. L., Signoretti, S., Look, A. T., Kung, A. L., von Boehmer, H., & Sicinski, P.
- Affiliations
- Harvard University (US)
- Boston Children's Hospital (US)
- Dana-Farber Cancer Institute (US)
- Brigham and Women's Hospital (US)
- ORCID
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2012-10
- Volume
- 22
- Issue
- 4
- Pages
- 438-451
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC3487466
- OpenAlex
- W2126821691
- Cited by
- 342
- References
- 56
- Citations by year
- 2026: 10 · 2025: 14 · 2024: 23 · 2023: 27 · 2022: 30 · 2021: 20 · 2020: 31 · 2019: 29 · 2018: 32 · 2017: 36 · 2016: 24 · 2015: 19 · 2014: 27 · 2013: 17 · 2012: 3
- FWCI
- 10.45
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 380 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (P01 CA080111, P01 CA109901, R01 CA083688)
- National Cancer Institute (1K99CA157951)
- Novartis
- Children’s Leukemia Research Association
- Japan Society for the Promotion of Science
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Keywords
- cyclin D1, cyclin D3, tumor maintenance, cell cycle, tumor cell senescence, apoptosis, breast cancer, targeted cancer therapy
- MeSH terms
- Animals, Female, Humans, Mammary Neoplasms, Experimental, Neoplasms, Apoptosis, Erb-b2 Receptor Tyrosine Kinases, Receptor, ErbB-2, Cyclin-Dependent Kinase 4, Mice, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma, Cyclin D, Cell Cycle Checkpoints
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