Mechanisms of transformation by the BCR-ABL oncogene: new perspectives in the post-imatinib era.
Since its introduction less than 3 years ago, imatinib mesylate (STI571) has altered the entire approach to the therapy of patients with chronic myeloid leukemia (CML). In addition to its impact on clinical practice, imatinib has also increased the focus of basic and translational CML research on enhancing the cellular effects of imatinib and preventing and overcoming resistance to the drug. Here, I summarize some recent advances in our understanding of the regulatory and signaling mechanisms of Bcr-Abl, with an emphasis on therapeutic implications.
Van Etten
Richard A
RA
Molecular Oncology Research Institute, Tufts-New England Medical Center, 750 Washington Street, Boston, MA 02111, USA. rvanetten@tufts-nemc.edu
D001549:Benzamides; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D016044:Fusion Proteins, bcr-abl / Q000235:genetics / Q000378:metabolism; D016313:Genes, abl / Q000502:physiology*; D006801:Humans; D000068877:Imatinib Mesylate; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy / Q000209:etiology / Q000235:genetics; D010879:Piperazines / Q000627:therapeutic use; D011743:Pyrimidines / Q000627:therapeutic use; D015398:Signal Transduction
D001549:Benzamides; D010879:Piperazines; D011743:Pyrimidines; D000068877:Imatinib Mesylate; D016044:Fusion Proteins, bcr-abl