The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.
Overview of cyclins D1 function in cancer and the CDK inhibitor landscape: past and present
Abstract
INTRODUCTION: Intensive efforts, over the last decade, have been made to inhibit the kinase activity of cyclins that act as mediators during cell-cycle progression. Activation of the cyclin D1 oncogene, often by amplification or rearrangement, is a major driver of multiple types of human tumors including breast and squamous cell cancers, B-cell lymphoma, myeloma and parathyroid adenoma. AREAS COVERED: In this review, the authors summarize the activity of cyclins and cyclin-dependent kinases in cell-cycle progression and transcription. They focus on cyclin D1/CDK4/CDK6, a central mediator in the transition from G1 to S phase. Furthermore, the authors discuss the first generation of pan-cyclin-dependent kinase inhibitors that failed to meet expectation and discuss, in detail, the second generation of highly specific cyclin D1/CDK4/CDK6 inhibitors that are proving to be more efficacious. EXPERT OPINION: The mechanism by which cyclin D1 drives tumorigenesis may be dependent on kinase and kinase-independent functions. Further evidence is necessary to delineate the roles of cyclin D1 in early pre-neoplastic lesions where its overexpression may promote genomic instability in a kinase-independent manner.
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Citations
Cites
Cell cycle, CDKs and cancer: a changing paradigm
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“There are 11 classical CDKs that can be divided into 2 groups based on their roles in cell-cycle progression or transcription [5,6].”
BackgroundThe DNA damage response: putting checkpoints in perspective
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A census of human cancer genes
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Blinded by the Light: The Growing Complexity of p53
Vousden, K. H., & Prives, C. (2009) · Cell · doi:10.1016/j.cell.2009.04.037 · Cited by 3,163
Glycogen synthase kinase-3β regulates cyclin D1 proteolysis and subcellular localization
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New functional activities for the p21 family of CDK inhibitors.
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“The inhibitory activity of Rb is modulated by sequential phosphorylation events by CDK4/6-Cyclin D and CDK2-Cyclin E, leading to release of E2F transcription factors to activate genes necessary for entry into S-phase DNA replication [10,11].”
BackgroundThe Rb/E2F pathway: expanding roles and emerging paradigms
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“p27 and p21 are CDK inhibitors; however, their association with cyclin D-cdk4/6 is implicated in the assembly and nuclear import of the cyclin D1 holoenzyme [75-77].”
Background
Cited by
FDA-approved small-molecule kinase inhibitors
Wu, P., Nielsen, T. E., & Clausen, M. H. (2015) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2015.04.005 · Cited by 1,013
Cyclin D1, cancer progression, and opportunities in cancer treatment
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Metadata
- Authors
- Casimiro, M. C., Velasco-Velázquez, M., Aguirre-Alvarado, C., & Pestell, R. G.
- Venue
- Expert Opinion on Investigational Drugs
- Publisher
- Informa UK Limited
- Published
- 2014-01-03
- Volume
- 23
- Issue
- 3
- Pages
- 295-304
- ISSN
- 1354-3784 (ISSN-L)
- 1744-7658
- OpenAlex
- W2019956469
- Cited by
- 184
- References
- 16
- FWCI
- 12.06
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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