Abstract
Pathogenesis of acute promyelocytic leukemia appears to be one of the best understood among human malignancies. The ability of retinoic acid (RA) and arsenic trioxide to directly target the oncogenic promyelocytic leukemia-retinoic receptor A (PML-RARA) fusion protein also made this disease the first model for oncogene-targeted therapies. A set of recent data has significantly increased the complexity of our view of acute promyelocytic leukemia pathogenesis, as well as of therapeutic response. This review summarizes and discusses these findings, which yield novels questions and models.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Arsenic Trioxide
-
Arsenicals / pharmacology
-
Arsenicals / therapeutic use*
-
Humans
-
Leukemia, Promyelocytic, Acute / drug therapy*
-
Leukemia, Promyelocytic, Acute / genetics
-
Leukemia, Promyelocytic, Acute / pathology
-
Models, Biological
-
Oncogene Proteins, Fusion / antagonists & inhibitors
-
Oncogene Proteins, Fusion / genetics
-
Oncogene Proteins, Fusion / metabolism
-
Oxides / pharmacology
-
Oxides / therapeutic use*
-
Tretinoin / pharmacology
-
Tretinoin / therapeutic use*
Substances
-
Arsenicals
-
Oncogene Proteins, Fusion
-
Oxides
-
promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
-
Tretinoin
-
Arsenic Trioxide