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.
MeSH Terms
Anticarcinogenic Agents/pharmacology,therapeutic use
Antineoplastic Agents/pharmacology,therapeutic use
Apoptosis/drug effects
Cell Differentiation/drug effects
Dimerization
Forecasting
Gene Expression Regulation, Neoplastic/drug effects
Humans
Leukemia, Promyelocytic, Acute/drug therapy,genetics
Models, Biological
Morphogenesis/drug effects
Neoplasm Proteins/antagonists & inhibitors,genetics,physiology
Neoplasms/drug therapy,genetics,prevention & control
Oncogene Proteins, Fusion/antagonists & inhibitors,genetics,physiology
Receptor Cross-Talk
Receptors, Retinoic Acid/chemistry,drug effects,physiology
Retinoids/chemistry,pharmacology,therapeutic use
Skin Neoplasms/chemically induced,genetics,prevention & control
Structure-Activity Relationship
Transcription Factor AP-1/antagonists & inhibitors
Transcriptional Activation/drug effects
Vitamin A/pharmacokinetics,physiology
Chemicals
Anticarcinogenic Agents
Antineoplastic Agents
Neoplasm Proteins
Oncogene Proteins, Fusion
Receptors, Retinoic Acid
Retinoids
Transcription Factor AP-1
promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
Vitamin A
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Altucci L
Dipartimento di Patologia Generale e Oncologia, Seconda Università degli Studi di Napoli, Italy. lucia.altucci@unina2.it
Gronemeyer H