Recent advancements in the treatment of chronic myelogenous leukemia.
Chronic myelogenous leukemia (CML) is a clonal hematopoetic stem cell disorder characterized by the Philadelphia chromosome and resultant production of the constitutively activated Bcr-Abl tyrosine kinase. Characterized clinically by marked myeloid proliferation, it invariably terminates in an acute leukemia. Conventional therapeutic options include interferon-based regimens and stem cell transplantation, with stem cell transplantation being the only curative therapy. Through rational drug development, STI571, a Bcr-Abl tyrosine kinase inhibitor, has emerged as a paradigm for gene product targeted therapy, offering new hope for expanded treatment options for patients with CML.
O'Dwyer
Michael E
ME
Leukemia Center, Oregon Cancer Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, Oregon 97201, USA. odwyerm@ohsu.edu
Mauro
Michael J
MJ
Druker
Brian J
BJ
D000970:Antineoplastic Agents / Q000627:therapeutic use; D001549:Benzamides; D004789:Enzyme Activation; D016044:Fusion Proteins, bcr-abl; D018380:Hematopoietic Stem Cell Transplantation; D006801:Humans; D000068877:Imatinib Mesylate; D007372:Interferons / Q000627:therapeutic use; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000175:diagnosis / Q000235:genetics / Q000628:therapy*; D010879:Piperazines / Q000627:therapeutic use; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors / Q000235:genetics; D011743:Pyrimidines / Q000627:therapeutic use
D000970:Antineoplastic Agents; D001549:Benzamides; D010879:Piperazines; D011743:Pyrimidines; D000068877:Imatinib Mesylate; D007372:Interferons; D011505:Protein-Tyrosine Kinases; D016044:Fusion Proteins, bcr-abl