Abstract
Retinoids have a reputation for being both detrimental and beneficial: they are teratogens, but they also have tumour-suppressive capacity. Cell biology and genetics have significantly improved our understanding of the mechanisms that underlie the anti-proliferative action of retinoids. Recent elucidation of the pathways that are activated by retinoids will help us to exploit the beneficial aspects of this powerful class of compounds for cancer therapy and prevention.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Anticarcinogenic Agents / pharmacology
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Anticarcinogenic Agents / therapeutic use
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Antineoplastic Agents / pharmacology
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Antineoplastic Agents / therapeutic use
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Apoptosis / drug effects
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Cell Differentiation / drug effects
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Dimerization
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Forecasting
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Gene Expression Regulation, Neoplastic / drug effects
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Humans
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Leukemia, Promyelocytic, Acute / drug therapy
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Leukemia, Promyelocytic, Acute / genetics
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Models, Biological
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Morphogenesis / drug effects
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Neoplasm Proteins / antagonists & inhibitors
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Neoplasm Proteins / genetics
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Neoplasm Proteins / physiology
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Neoplasms / drug therapy*
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Neoplasms / genetics
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Neoplasms / prevention & control
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Oncogene Proteins, Fusion / antagonists & inhibitors
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Oncogene Proteins, Fusion / genetics
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Oncogene Proteins, Fusion / physiology
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Receptor Cross-Talk
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Receptors, Retinoic Acid / chemistry
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Receptors, Retinoic Acid / drug effects
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Receptors, Retinoic Acid / physiology
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Retinoids / chemistry
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Retinoids / pharmacology
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Retinoids / therapeutic use*
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Skin Neoplasms / chemically induced
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Skin Neoplasms / genetics
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Skin Neoplasms / prevention & control
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Structure-Activity Relationship
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Transcription Factor AP-1 / antagonists & inhibitors
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Transcriptional Activation / drug effects
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Vitamin A / pharmacokinetics
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Vitamin A / physiology
Substances
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Anticarcinogenic Agents
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Antineoplastic Agents
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Neoplasm Proteins
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Oncogene Proteins, Fusion
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Receptors, Retinoic Acid
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Retinoids
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Transcription Factor AP-1
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promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
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Vitamin A