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The cell cycle: a review of regulation, deregulation and therapeutic targets in cancer

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TLDR
This review provides an overview of deregulation of the cell cycle in cancer by focusing on mechanisms, i.e. regulation of cyclin‐dependent kinases (CDK) by cyclins, CDK inhibitors and phosphorylating events.
Abstract
The cell cycle is controlled by numerous mechanisms ensuring correct cell division. This review will focus on these mechanisms, i.e. regulation of cyclin-dependent kinases (CDK) by cyclins, CDK inhibitors and phosphorylating events. The quality checkpoints activated after DNA damage are also discussed. The complexity of the regulation of the cell cycle is also reflected in the different alterations leading to aber- rant cell proliferation and development of cancer. Consequently, targeting the cell cycle in general and CDK in particular presents unique opportunities for drug discovery. This review provides an overview of deregulation of the cell cycle in cancer. Different families of known CDK inhibitors acting by ATP competition are also discussed. Cur- rently, at least three compounds with CDK inhibitory activity (flavopiridol, UCN-01, roscovitine) have entered clinical trials.

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Therapeutic microRNA Delivery Suppresses Tumorigenesis in a Murine Liver Cancer Model

TL;DR: It is demonstrated that hepatocellular carcinoma (HCC) cells exhibit reduced expression of miR-26a, a miRNA that is normally expressed at high levels in diverse tissues that may provide a general strategy for miRNA replacement therapies.
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Regulation of DNA repair throughout the cell cycle

TL;DR: The repair of DNA lesions that occur endogenously or in response to diverse genotoxic stresses is indispensable for genome integrity and has provided insights into the mechanisms that contribute to DNA repair in specific cell-cycle phases.
Journal ArticleDOI

Natural products to drugs: natural product derived compounds in clinical trials

TL;DR: Natural product and natural product-derived compounds that are being evaluated in clinical trials or are in registration (as at 31st December 2007) have been reviewed, as well as natural products for which clinical trials have been halted or discontinued since 2005.
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Ferulic Acid: Therapeutic Potential Through Its Antioxidant Property

TL;DR: The present review deals with the mechanism of antioxidant property of FA and its possible role in therapeutic usage against various diseases.
Journal ArticleDOI

The regulation of cyclin D1 degradation: roles in cancer development and the potential for therapeutic invention.

TL;DR: Current knowledge on the regulation of cyclin D1 degradation is discussed and novel insights into cyclinD1 degradation are also discussed in the context of ablative therapy.
References
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Journal ArticleDOI

WAF1, a potential mediator of p53 tumor suppression

TL;DR: A gene is identified, named WAF1, whose induction was associated with wild-type but not mutant p53 gene expression in a human brain tumor cell line and that could be an important mediator of p53-dependent tumor growth suppression.
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p53 mutations in human cancers

TL;DR: The p53 mutational spectrum differs among cancers of the colon, lung, esophagus, breast, liver, brain, reticuloendothelial tissues, and hemopoietic tissues as mentioned in this paper.
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p53, the Cellular Gatekeeper for Growth and Division

TL;DR: The author regrets the lack of citations for many important observations mentioned in the text, but their omission is made necessary by restrictions in the preparation of review manuscripts.
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Mutation and Cancer: Statistical Study of Retinoblastoma

TL;DR: The hypothesis is developed that retinoblastoma is a cancer caused by two mutational events, in the dominantly inherited form, one mutation is inherited via the germinal cells and the second occurs in somatic cells.
Journal ArticleDOI

Cancer Cell Cycles

TL;DR: Genetic alterations affecting p16INK4a and cyclin D1, proteins that govern phosphorylation of the retinoblastoma protein and control exit from the G1 phase of the cell cycle, are so frequent in human cancers that inactivation of this pathway may well be necessary for tumor development.