title: The biology of acute promyelocytic leukemia.
abstract: Acute promyelocytic leukemia (APL) is a disease associated with fusion oncoproteins invariably involving the retinoic acid receptor (Raralpha). Retinoic acid induces differentiation in APL cells and is successfully used in conjunction with chemotherapy to treat and cure a significant percentage of patients with APL. APL is also a model for disruption of normal retinoid-mediated transcription resulting in blocked differentiation. The study of the molecular mechanisms of APL oncogenesis has revealed novel interactions between fusion oncoproteins and transcriptional coregulators, already leading to new treatment strategies.
authors: Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish General Hospital, 3755 Cote Ste. Catherine Road, Montreal, Quebec, Canada.
authors: K K
authors: KK
authors: Mann
authors: W
authors: W
authors: Shao
authors: W H
authors: WH
authors: Miller
mesh_terms: D000818:Animals; D019008:Drug Resistance, Neoplasm; D006801:Humans; D015473:Leukemia, Promyelocytic, Acute / Q000188:drug therapy / Q000235:genetics* / Q000503:physiopathology; D051379:Mice; D023421:Models, Animal; D009363:Neoplasm Proteins / Q000502:physiology*; D015514:Oncogene Proteins, Fusion / Q000502:physiology*; D018168:Receptors, Retinoic Acid / Q000235:genetics* / Q000502:physiology; D014212:Tretinoin / Q000627:therapeutic use
chemical_list: D009363:Neoplasm Proteins; D015514:Oncogene Proteins, Fusion; D018168:Receptors, Retinoic Acid; C093476:promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; D014212:Tretinoin