Abstract
Acute myelogenous leukemia (AML) is a difficult disease to treat. Novel treatment strategies, including molecular targeted therapy, are being explored. The c-kit receptor represents a potential therapeutic target for AML. The receptor is expressed on more than 10% of blasts in 64% of patients with de novo AML and 95% of those with relapsed AML. It mediates proliferation and anti-apoptotic effects in AML. This review discusses the biology of c-kit in normal and malignant hematopoiesis and the recent clinical trials targeting c-kit in AML.
MeSH terms
-
Aged
-
Antineoplastic Agents / pharmacology*
-
Antineoplastic Agents / therapeutic use
-
Apoptosis / drug effects
-
Apoptosis / physiology
-
Cell Division / drug effects
-
Cell Division / physiology
-
Clinical Trials as Topic
-
Drug Delivery Systems
-
Drug Resistance, Neoplasm / genetics
-
Hematopoiesis / drug effects
-
Hematopoiesis / physiology
-
Hematopoietic Stem Cells / drug effects
-
Hematopoietic Stem Cells / enzymology
-
Humans
-
Leukemia, Myeloid, Acute / drug therapy*
-
Leukemia, Myeloid, Acute / enzymology
-
Leukemia, Myeloid, Acute / genetics
-
Middle Aged
-
Multicenter Studies as Topic
-
Neoplasm Proteins / antagonists & inhibitors*
-
Neoplasm Proteins / genetics
-
Neoplasm Proteins / physiology
-
Neoplastic Stem Cells / drug effects
-
Neoplastic Stem Cells / enzymology
-
Protein Kinase Inhibitors / pharmacology*
-
Protein Kinase Inhibitors / therapeutic use
-
Proto-Oncogene Proteins c-kit / antagonists & inhibitors*
-
Proto-Oncogene Proteins c-kit / genetics
-
Proto-Oncogene Proteins c-kit / physiology
Substances
-
Antineoplastic Agents
-
Neoplasm Proteins
-
Protein Kinase Inhibitors
-
Proto-Oncogene Proteins c-kit