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Targeting cell cycle regulation in cancer therapy.

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TLDR
An overview on the role of CDK-cyclin complexes, metabolic adaptations and oxidative stress in regulating progression through each cell cycle phase and transitions between them is provided.
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This article is published in Pharmacology & Therapeutics.The article was published on 2013-05-01. It has received 292 citations till now. The article focuses on the topics: Cell cycle phase & Cell cycle.

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Sustained proliferation in cancer: Mechanisms and novel therapeutic targets

TL;DR: Natural compounds found to inhibit one or more pathways that contribute to proliferation have been found and will be very important for identifying signaling pathways and molecular targets that may provide early diagnostic markers and/or critical targets for the development of new drugs or drug combinations that block tumor formation and progression.
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How the Warburg effect supports aggressiveness and drug resistance of cancer cells

TL;DR: In depth understanding of these metabolic changes in cancer cells may lead to the development of novel therapeutic strategies, which when combined with existing cancer treatments, might improve their effectiveness and/or overcome chemoresistance.
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Essential Oils and Their Constituents as Anticancer Agents: A Mechanistic View

TL;DR: The current review indicates that EOs and their constituents act by multiple pathways and mechanisms involving apoptosis, cell cycle arrest, antimetastatic and antiangiogenic, increased levels of reactive oxygen and nitrogen species (ROS/RNS), DNA repair modulation, and others to demonstrate their antiproliferative activity in the cancer cell.
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Arsenic exposure: A public health problem leading to several cancers.

TL;DR: The present review outlines of arsenic toxic effects focusing on different cancer types whit highest prevalence's by exposure to this metalloid and signaling pathways of carcinogenesis.
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Interconnection between Metabolism and Cell Cycle in Cancer.

TL;DR: Targeting a few metabolic enzymes also periodically translocate to the nucleus and oversee cell cycle regulators or oncogene expression could increase the response to CDK inhibitors (CKIs).
References
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Journal ArticleDOI

Hallmarks of cancer: the next generation.

TL;DR: Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer.
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Surfing the p53 network

TL;DR: The p53 tumour-suppressor gene integrates numerous signals that control cell life and death, and the disruption of p53 has severe consequences when a highly connected node in the Internet breaks down.
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CDK inhibitors: positive and negative regulators of G1-phase progression

TL;DR: This work challenges previous assumptions about how the G1/S transition of the mammalian cell cycle is governed, helps explain some enigmatic features of cell cycle control that also involve the functions of the retinoblastoma protein (Rb) and the INK4 proteins, and changes the thinking about how either p16 loss or overexpression of cyclin D-dependent kinases contribute to cancer.
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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.
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In vivo activation of the p53 pathway by small-molecule antagonists of MDM2.

TL;DR: In this article, the authors identify potent and selective small-molecule antagonists of MDM2 and confirm their mode of action through the crystal structures of complexes, leading to cell cycle arrest, apoptosis, and growth inhibition of human tumor xenografts.
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