Abstract
Tumour cells undergo uncontrolled proliferation, yet tumours most often originate from adult tissues, in which most cells are quiescent. So, the proliferative advantage of tumour cells arises from their ability to bypass quiescence. This can be due to increased mitogenic signalling and/or alterations that lower the threshold required for cell-cycle commitment. Understanding the molecular mechanisms that underlie this commitment should provide important insights into how normal cells become tumorigenic and how new anticancer strategies can be devised.
MeSH terms
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Animals
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Antineoplastic Agents / pharmacology
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CDC2-CDC28 Kinases*
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Cell Cycle Proteins / genetics
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Cell Cycle Proteins / physiology*
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Cell Cycle*
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Cell Differentiation / physiology
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Cell Division / genetics
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Cell Transformation, Neoplastic / genetics
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Cell Transformation, Neoplastic / pathology*
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Cyclin-Dependent Kinase 2
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Cyclin-Dependent Kinases / antagonists & inhibitors
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Cyclin-Dependent Kinases / genetics
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Cyclin-Dependent Kinases / physiology
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Cyclins / genetics
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Cyclins / physiology
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Drug Design
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Enzyme Inhibitors / pharmacology
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Enzyme Inhibitors / therapeutic use
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G1 Phase / physiology
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Genes, Tumor Suppressor
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Genes, cdc
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Humans
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Mice
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Mice, Knockout
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Models, Animal
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Models, Biological
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Mutation
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Neoplasm Proteins / physiology
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Neoplasms / genetics
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Neoplasms / pathology*
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Protein Serine-Threonine Kinases / physiology
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Signal Transduction
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Substrate Specificity
Substances
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Antineoplastic Agents
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Cell Cycle Proteins
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Cyclins
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Enzyme Inhibitors
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Neoplasm Proteins
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Protein Serine-Threonine Kinases
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CDC2-CDC28 Kinases
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CDK2 protein, human
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Cdk2 protein, mouse
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Cyclin-Dependent Kinase 2
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Cyclin-Dependent Kinases